0% found this document useful (0 votes)
41 views14 pages

Beverages: An Update On The Health Benefits of Green Tea

Benifits of taking green tea

Uploaded by

Deepak Yadav
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
41 views14 pages

Beverages: An Update On The Health Benefits of Green Tea

Benifits of taking green tea

Uploaded by

Deepak Yadav
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 14

beverages

Review
An Update on the Health Benefits of Green Tea
Wanda C. Reygaert
Oakland University William Beaumont School of Medicine, Rochester, MI 48309, USA;
reygaert@oakland.edu; Tel.: +1-248-370-2709

Academic Editor: Quan V. Vuong


Received: 21 June 2016; Accepted: 19 December 2016; Published: 18 January 2017

Abstract: Green tea, which is produced from the leaves of the Camellia sinensis plant, is one of the
most popular beverages worldwide. Over the past 30 years or more, scientists have studied this
plant in respect to potential health benefits. Research has shown that the main components of green
tea that are associated with health benefits are the catechins. The four main catechins found in
green tea are: (−)-epicatechin (EC), (−)-epicatechin-3-gallate (ECG), (−)-epigallocatechin (EGC), and
(−)-epigallocatechin-3-gallate (EGCG). Of these four, EGCG is present in the largest quantity, and so
has been used in much of the research. Among the health benefits of green tea are: anticarcinogenic,
anti-inflammatory, antimicrobial, and antioxidant properties, and benefits in cardiovascular disease
and oral health. Research has been carried out using various animal models and cells lines, and
is now more and more being carried out in humans. This type of research will help us to better
understand the direct benefits of green tea. This review will focus primarily on research conducted
using human subjects to investigate the health benefits of green tea.

Keywords: green tea; anticarcinogenic; anti-inflammatory; antimicrobial; antioxidant; cardiovascular


disease; oral health

1. Introduction
Tea is a popular drink worldwide. Cultivation of tea plants is economically important in many
countries, and the tea plant, Camellia sinensis (Figure 1), is known to be grown in as many as 30 countries.
Camellia sinensis grows best in certain tropical and subtropical regions [1]. There are four main types of
tea produced from this same plant, depending on how the tea leaves are processed. These teas are
white, green, Oolong, and black tea. White tea is produced from very young leaves and buds that have
not yet turned green, and the only processing is drying. Green tea is produced from mature leaves with
minimal processing (only drying). Oolong tea is produced from partially fermented mature leaves,
and black tea is produced from fully fermented mature leaves [1,2]. Green tea, which makes up around
20% of tea production worldwide, is consumed most often in China, Korea, and Japan. Oolong tea is
consumed most in China and Taiwan. Black tea (around 78% of tea production) is mostly consumed in
the United States and the United Kingdom. Black tea contains up to three times the amount of caffeine
as green tea [3–5].
The components of green tea that are the most relevant medically are the polyphenols, with the
flavonoids being the most important. The most pertinent flavonoids are the catechins, which make up
80%–90% of the flavonoids, and approximately 40% of the water-soluble solids in green tea [6–8].
The amount of catechins in the tea can be affected by which leaves are harvested, how the leaves are
processed, and how the tea is prepared. In addition, where the leaves are grown (geographically)
and the growing conditions affect catechin amounts [3,9–12]. Polyphenols are quickly oxidized after
harvesting due to the enzyme polyphenol oxidase. To prevent loss of the polyphenols, green tea
leaves are heated rapidly (most commonly by steaming or pan frying) to inactivate polyphenol
oxidase. Black tea leaves are dried, then rolled and crushed, which promotes oxidation. Therefore,

Beverages 2017, 3, 6; doi:10.3390/beverages3010006 www.mdpi.com/journal/beverages


Beverages 2017, 3, 6 2 of 14

Beverages 2017, 3, 6   2 of 13 
Beverages 2017, 3, 6  
black tea has far fewer active catechins than green tea [1,2,5,8]. Green tea contains four 2 of 13  main
catechins: ( − )-epicatechin (EC), ( − )-epigallocatechin (EGC), ( − )-epicatechin-3-gallate (ECG),
black tea has far fewer active catechins than green tea [1,2,5,8]. Green tea contains four main catechins:  and
black tea has far fewer active catechins than green tea [1,2,5,8]. Green tea contains four main catechins: 
−)-epigallocatechin-3-gallate
((−)‐epicatechin  (EGCG). The most(EGC), 
(EC),  (−)‐epigallocatechin  abundant of these in green tea is EGCG,
(−)‐epicatechin‐3‐gallate  (ECG),  which
and 
(−)‐epicatechin  (EC),  (−)‐epigallocatechin  (EGC),  (−)‐epicatechin‐3‐gallate  (ECG),  and 
represents around 59% of total
(−)‐epigallocatechin‐3‐gallate  catechins.
(EGCG).  The abundant 
The  most  next mostof  abundant
these  in isgreen 
EGC tea 
(around 19%),which 
is  EGCG,  then
(−)‐epigallocatechin‐3‐gallate  (EGCG).  The  most  abundant  of  these  in  green  tea  is  EGCG,  which 
ECG (around 14%), and EC (around 6%) [2,3,8]. Figure 2 shows a representation of green tea
represents around 59% of total catechins. The next most abundant is EGC (around 19%), then ECG 
represents around 59% of total catechins. The next most abundant is EGC (around 19%), then ECG 
catechin composition.
(around  14%),  and  EC  (around  6%)  [2,3,8].  Figure  2  shows  a  representation  of  green  tea  catechin 
(around  14%),  and  EC  (around  6%)  [2,3,8].  Figure  2  shows  a  representation  of  green  tea  catechin 
composition. 
composition. 

 
 
Figure 1. Drawing of the Camellia sinensis plant. 
Figure 1. Drawing of the Camellia sinensis plant.
Figure 1. Drawing of the Camellia sinensis plant. 

 
 
Figure 2. Relative composition of green tea catechins. 
Figure 2. Relative composition of green tea catechins. 
Figure 2. Relative composition of green tea catechins.
The health benefits of green tea depend on its bioavailability after consumption. In the body, 
The health benefits of green tea depend on its bioavailability after consumption. In the body, 
The health benefits of green tea depend on its bioavailability after consumption. In the body,
the  components  in  green  tea  may  undergo  metabolic  processing  such  as  glucuronidation, 
the 
the components 
components in in 
greengreen 
tea tea  undergo
may may  undergo  metabolic 
metabolic processing 
processing such as such  as  glucuronidation, 
glucuronidation, methylation,
methylation,  and  sulfation,  which  produces  active  metabolites  [13].  The  catechins  and  their 
methylation, 
and sulfation,and 
which sulfation, 
produceswhich 
activeproduces 
metabolites active 
[13]. metabolites 
The catechins [13]. 
andThe theircatechins 
metabolitesand 
may their 
be
metabolites may be detected in blood plasma, urine, and various tissues. Studies on bioavailability 
metabolites may be detected in blood plasma, urine, and various tissues. Studies on bioavailability 
detected in blood plasma, urine, and various tissues. Studies on bioavailability are often conducted
are often conducted collecting specimens at timed intervals (after ingestion). Various studies have 
are often conducted collecting specimens at timed intervals (after ingestion). Various studies have 
collecting specimens at normally 
timed intervals (after ingestion). Various [14–16], 
studies have been green 
conducted using
been  conducted  using  prepared  green  tea  beverages  ingested  tea  extract 
been  conducted  using  normally  prepared  green  tea  beverages  [14–16],  ingested  green 
normally prepared green tea beverages [14–16], ingested green tea extract (total catechins) [14,17,18], tea  extract 
(total catechins) [14,17,18], or ingestion of specific catechins [19–21]. These studies have shown that 
(total catechins) [14,17,18], or ingestion of specific catechins [19–21]. These studies have shown that 
or ingestion of specific catechins [19–21]. These studies have shown that ECG and EGCG, and
ECG and EGCG, and metabolites of EC and EGC can be detected and measured in blood plasma. In 
ECG and EGCG, and metabolites of EC and EGC can be detected and measured in blood plasma. In 
metabolites of EC and EGC can be detected and measured in blood plasma. In urine, only metabolites of
urine, only metabolites of EC and EGC can be detected. Peak concentrations of components in blood 
urine, only metabolites of EC and EGC can be detected. Peak concentrations of components in blood 
EC and EGC
plasma  can be occur 
generally  detected. Peak2 concentrations
about  of components
h  after  ingestion.  in blood plasma
Peak  concentrations  generally occur
of  components  in  about
urine 
plasma  generally  occur  about  2  h  after  ingestion.  Peak  concentrations  of  components  in  urine 
2 h after ingestion. Peak concentrations of components in urine generally occur
generally occur between 4–6 h after ingestion. Certain studies have been conducted using various between 4 and 6h
generally occur between 4–6 h after ingestion. Certain studies have been conducted using various 
after ingestion. Certain studies have been conducted using various concentrations of catechins,
concentrations  of  catechins,  and  generally  show  that  the  bioavailability  of  these  substances  is  in 
concentrations  of  catechins,  and  generally  show  that  the  bioavailability  of  these  substances  is  in 
and generally show that the bioavailability of these substances is in proportion to the amount
proportion to the amount ingested [18,19,22–24]. It has been suggested that levels of EC and ECG 
proportion to the amount ingested [18,19,22–24]. It has been suggested that levels of EC and ECG 
detected are too low to be of any therapeutic value, so most research considers only EGC and EGCG 
detected are too low to be of any therapeutic value, so most research considers only EGC and EGCG 
[25]. Table 1 shows a summary of the results of some of these studies. 
[25]. Table 1 shows a summary of the results of some of these studies. 
Beverages 2017, 3, 6 3 of 14

ingested [18,19,22–24]. It has been suggested that levels of EC and ECG detected are too low to
be of any therapeutic value, so most research considers only EGC and EGCG [25]. Table 1 shows
a summary of the results of some of these studies.

Table 1. Green tea catechin bioavailability studies summary.

Plasma Concentration EGC in Urine/24 h


Source Initial Dose Ingested References
(Peak Time) (Peak Time)
EGCG 230–235 µmol EGCG 55 nmol/L (1.9 h) [15]
Green tea beverage 33 µmol
EGC 257–260 µmol EGC 126–205 nmol/L (2.2 h) [16]
EGCG 88–110 mg EGCG 119–135 ng/mL [17]
Green tea extracts 3.0 mg (3–6 h)
EGC 82–102 mg EGC 140–148 ng/mL [18]

Over the past 15–20 years, a number of other research studies have been conducted to determine
what health benefits can be attributed to consumption of green tea and its extracts. This research has
shown that green tea has a variety of potential health benefits. These benefits include anticarcinogenic,
anti-inflammatory, antimicrobial, and antioxidant properties, and benefits in cardiovascular disease
and oral health. While much of this research has been performed in vitro, and a significant amount of
the research done in vivo, using animal models, this paper will focus mainly on studies conducted
with human subjects (plus pertinent information from the other types of studies).

2. Anticarcinogenic Properties of Green Tea


Cancer is currently a major source of morbidity and mortality worldwide. Billions of dollars in
research monies have been poured into cancer research over the past 50 plus years, and yet we do not
seem to be any closer to actually curing it. In addition, quite often the chemotherapies do as much,
if not more damage to the patient as the disease. Because cancer appears in so many different forms in
multiple parts of the body, it has been difficult to determine the mechanisms that lead to the disease.
Even with what we now know about cancer risk factors, there are still many people who seemingly
have none of the risk factors, and yet succumb to a rapidly aggressive form. Encouraging people to
think about how a healthy lifestyle can prevent disease is certainly a step in the right direction, and it
would be most helpful to identify substances that could be useful in prevention and treatment.
The main component of green tea that has been studied in cancer research is EGCG. There are
several cancer related mechanisms attributed to EGCG. These include: inhibition of angiogenesis, DNA
hypermethylation, NF-κB, telomerase activity, and tumor cell proliferation and metastasis; induction
of tumor suppressor genes; and promotion of tumor cell apoptosis [26–30]. Inhibition of angiogenesis
is suggested to occur through a decrease in RNA and peptide levels of vascular endothelial growth
factor (VEGF), and by disrupting the dimerization of VEGF with the vascular endothelial growth factor
receptor 2 (VEFR2) [31]. Another suggested way in which green tea catechins may generally inhibit
carcinogenesis is through increasing levels of glutathione S-transferase pi (GST-pi), which catalyzes
detoxification reactions that inhibit carcinogen-induced DNA damage [32].
Analysis of studies performed using human oral consumption of green tea to assess cancer risk
showed that case-control studies gave the most consistent results and were positive for reduced
cancer risk in breast, cardiac, colorectal, esophageal, gastric, lung, ovarian, pancreatic, and prostate
cancers [33,34]. A recent large study showed a relationship between breast cancer risk and tea
consumption, with the risk being highest in the groups that did not consume tea and lowest in the
groups that consumed the most cups per day. Number of cups were assessed in five categories
(0.1–1.0 cups, 1.1–2.0 cups, 2.1–3.0 cups, 3.1–5.0 cups, >5.0 cups) [35]. Analysis of the types of green
tea beverage or extracts used in studies suggests that green tea beverage or a supplement containing
mixed catechins may be more effective than using single catechin (e.g., EGCG) supplements [36].
The potential molecular mechanisms and targets that might explain how green tea catechins
possess anticarcinogenic properties have been widely studied (using various cell cultures, etc.),
Beverages 2017, 3, 6 4 of 14

especially in breast cancers. These include interaction with specific proteins, anti-angiogenesis
mechanisms, targets for inhibition of enzyme activities and cell signaling pathways, and induction
of cell cycle arrest and apoptosis [37]. Table 2 gives a summary of some of these potential targets
and mechanisms.

Table 2. Potential targets and mechanisms of green tea catechins in breast cancer.

Source Molecule(s) Affected Pathway Result References


Inhibition of Cancer Cell Growth, Proliferation, Invasion
Silences 67LR by binding
67-kDa laminin receptor
EGCG to it which activates Inhibition of cell growth [38]
(67LR)
myosin phosphatase
Cyclin-dependent kinase 2 Inhibits activity of Cdk2
EGCG Cell cycle arrest at G1 [39]
(Cdk2) and 4 (Cdk4) and Cdk4
Dual-specificity
tyrosine-phosphorylated Decreased cell
EGCG Inhibits DYRK1A [40]
and regulated kinase 1A proliferation
(DYRK1A)
Epidermal growth factor Down regulates levels of Inhibition of cell growth
EGCG [41]
receptor (EGFR) EGFR protein and invasive activity
Estrogen receptor alpha Down regulates level of Inhibition of cell
EGCG [42]
(ER-α) ER-α protein proliferation
Increases levels of HBP1
HMG-Box transcription Inhibition of cell
EGCG which represses [43]
factor (HBP1) invasive activity
Wnt signaling
Human epidermal growth Inhibits phosphorylation
EGCG Inhibition of cell growth [44,45]
factor receptor 2 (HER-2) of HER-2
Inhibits HGF inducing
Hepatocyte growth factor Inhibition of cell motility
EGCG phosphorylation of its [46]
(HGF) and invasive activity
receptor (Met)
Inhibition of cell
Insulin-like growth factor-1 Binds to IGF-1R and
EGCG proliferation and [47]
receptor (IGF-1R) inhibits its kinase activity
transformation
Binds to PI3K kinase
Phosphoinositide-3-kinase Inhibition of cell
EGCG domain competing [48]
(PI3K) proliferation
with ATP
Decreased tumor cell
Green tea extract Vascular endothelial growth Inhibits transcription of blood vessel density,
[49–51]
(GTE) factor (VEGF) VEGF inhibition
of proliferation
Binds to vimentin
Intermediate filament Inhibition of cell
EGCG inhibiting its [52]
vimentin proliferation
phosphorylation
Induction of Apoptosis
B-cell lymphoma-extra large Binds in the P1 pocket Suppression of
EGCG [53]
protein (Bcl-xL ) of Bcl-xL anti-apoptosis
EGCG, green tea Caspase-3, -8, -9; tumor Increased expression of
Induction of apoptosis [54–56]
catechins protein 53 (p53) caspase-3, -8, -9, and p53
Glucose-regulated protein 78 Binds GPR78 at Suppression of
EGCG [57]
(GRP78) ATP-binding site anti-apoptosis

The mushrooming area of nanotechnology has lead to the development of potential chemotherapy
involving nanoparticles (NPs). Various particles (e.g., gold) can be used to deliver compounds to
specific areas of the body. Research using EGCG and nanoparticles has already begun using a number
of delivery approaches. These include: coating an NP, such as gold, with EGCG; use of encapsulated
(in liposomes or polymeric NPs) EGCG in NPs along with anti-cancer drugs, outer ligands that will
bind to specific targets, or outer polymers that will enhance the intestinal absorption of EGCG [30].
Beverages 2017, 3, 6 5 of 14

3. Cardiovascular Disease Health Benefits


Cardiovascular disease (CVD) is a complex disorder involving multiple factors. Among those
factors are inflammation, oxidative stress, platelet aggregation, and lipid metabolism. Some of these
factors are also involved in other disease processes, but will be discussed in this paper under CVD.
There have been a number of studies over the years assessing green tea consumption in respect to
CVD risk [58]. Two studies from Japan that included nearly 50,000 people found a decreased mortality
rate due to CVD based on consumption of various numbers of cups per day. One study showed a
28% decrease in CVD death between those who consumed ≤3 cups and those who consumed ≥10 cups.
The other study showed a 14% decrease in CVD mortality between those who consumed <1 cup and
those who consumed ≥5 cups [59,60]. Other studies in Japan using a green tea extract found that,
after 12 weeks, the subjects had reductions in body fat (10%), blood pressure (6.5%), and low-density
lipoprotein (LDL) levels (2.6%), suggesting reduced risk of CVD. After two months, diabetic patients
also had reduced fasting blood glucose levels (from 135 to 128.8 mg/dL), and hemoglobin A1c (HBA1c)
levels (from 6.2% to 6.0%) [61,62]. A large meta-analysis of 17 studies from over 30 years, including
data from Europe, the UK, and the U.S., found that increasing consumption of green tea by three
cups per day decreased the risk of myocardial infarction (MI) death by 11% [63]. Another study
showed a decreased risk of mortality in patients who had an acute MI and a history of regular green
tea consumption for at least a year prior to the MI. Participants who did not drink green tea had a
14% rate of death due to the MI; participants who drank up to 14 cups per week had an 11% rate of
MI death; and participants who drank more than 14 cups per week had a 10% rate of MI death [64].
An interesting study in patients with CVD showed that consumption of EGCG resulted in a rapid
improvement of vascular endothelial function. Participants who ingested an initial dose of 300 mg
of EGCG had an improved brachial artery flow-mediated dilation from 7.1% to 8.6% after 2 h [65].
Another recent study found that increased intake of dietary flavonoids was associated with a decreased
risk of CVD. The participants were divided into three groups based on average daily consumption of
flavonoids. The first tertile consumed 89 mg/day, the second tertile consumed 251 mg/day, and the
third tertile consumed 532 mg/day. The number of deaths due to CVD in the first tertile was 8.6%;
in the second tertile, 6.4%; and in the third tertile, 5.0% [66].

3.1. Inflammation
Besides CVD, inflammation is also involved in arthritis, aging, cancer, etc. Many of the
anti-inflammatory effects when using green tea have been studied in rheumatoid arthritis (RA) and
osteoarthritis (OA), and are pertinent to CVD as well. Some general anti-inflammatory mechanisms of
green tea components are: increased production of the anti-inflammatory cytokine, IL-10; regulation of
IL-6 synthesis and signaling; decreased production of destructive matrix metalloproteinases via TNF-α
induced phosphorylation of mitogen-activated protein kinases (MAPKs); and decreased expression
of the chemokine receptor CCR2 and decreased levels of the proinflammatory cytokines IL-1β and
TNF-α [2,67–70].
The specific studies on inflammation can be roughly categorized into: inhibition of
neutrophil-endothelium interaction, modulation of neutrophil functions and death, and regulation
of inflammation factors. Neutrophil migration and function is an integral part of the inflammatory
response, so controlling neutrophils is vital in decreasing inflammation. Studies have shown that
green tea catechins cause a reduction in the number of leukocyte-endothelial cell adhesion molecules
(CAMs), such as ICAM-1, VCAM-1, and E-selection, expressed on the endothelial cell surface.
This restricts the ability of the neutrophils to migrate to sites of infection [71,72]. Other studies
have shown that factors known to regulate neutrophil function, such as IL-1β, IL-2, TNF-α, and
granulocyte-macrophage colony-stimulating factor (GM-CSF), are suppressed by consumption of
green tea or EGCG, resulting in inhibition of inflammation [73–75]. Studies on the inhibition of
pro-inflammatory factors have shown that green tea catechins downregulate many inflammatory
Beverages 2017, 3, 6 6 of 14

chemokines, cytokines, and inflammatory markers such as: IL-1α, IL-1β, IL-6, IL-8, Interferon gamma
(INF-γ), and C-reactive protein (CRP) [74,76–78].

3.2. Oxidative Stress


Oxidative stress in the body is closely tied to inflammation and CVD, and is the result of
the damaging effects of reactive oxygen species (ROS). These ROS are capable of causing chronic
inflammation through induction of inflammatory cytokines and chemokines, and pro-inflammatory
transcription factors. In general, green tea catechins have been found to have antioxidant activity
through: inhibiting redox sensitive transcription factors and pro-oxidant enzymes, scavenging ROS,
and inducing anti-oxidant enzymes [8].
Studies to determine the antioxidant capabilities of green tea may measure a variety of substances.
Tests may measure the presence of known ROS or their metabolites, such as hydroxyl radical, peroxides,
superoxide, and singlet oxygen. Other measurements may be for known antioxidant substances such
as superoxide dismutase (SOD) and glutathione peroxidase, or substances that indicate inflammation
such as high-sensitivity C-reactive protein (hs-CRP) and TNF-α. Another type of testing assesses total
antioxidant capacity (TAC), also known as total antioxidant status (TAS), which measures the amount
of oxidants that are neutralized in the body (e.g., moles of oxidant neutralized by 1 L of plasma),
with a lower number translating into a higher risk of disease [67].
The results from recent studies have shown that green tea catechins can affect levels of ROS [79–82],
increase levels of antioxidants [83–86], decrease levels of inflammatory substances [87,88], and increase
TAC (TAS) [84,86,87]. An excellent summary of earlier studies that measured ROS and TAC can be
found in a chapter by Serafini et al. 2011 [67].

3.3. Platelet Aggregation


Platelet activation and subsequent aggregation play an important role in CVD. When the vascular
endothelium is damaged, platelets usually respond rapidly and aggregate to form plugs at the damage
site, and may also form clots that could lead to vessel occlusion [8,89]. Many of the studies on
platelet aggregation have been carried out using various animal platelets. In addition to showing
that green tea catechins were involved in inhibition of platelet aggregation, studies suggested that
catechins may affect several cellular targets that are related to platelet activation, including: through
the arachadonic acid pathway, inhibition of a cytoplasmic increase in calcium, decreased thrombaxane
A2 (TXA2 ) production, and inhibition of cyclooxygenase-1 (COX)-1 [90–93]. A study using human
platelets concluded that EGCG was able to inhibit platelet activation by adenosine diphosphate (ADP)
stimulation, and suppressed the p38 MAPK phosphorylation of heat shock protein 27 (HSP27), which
would inhibit the release of pro-thrombotic contents from platelets [94].

3.4. Lipid Metabolism


Increased blood lipid levels have long been suspected as an increased risk for CVD, especially
LDLs [95]. One mechanism that is linked with atherosclerosis is the presence of oxidated LDL [96].
There have been many studies performed using humans subjects to determine the effect of green tea
catechins on lipids. The studies have reported that consumption of green tea catechins lowers total
cholesterol and LDL levels and also reduces blood pressure [87,97–104]. In addition, a recent study
found that green tea catechins are incorporated into LDL particles, and are then able to reduce the
oxidation of LDL. Catechins prevent LDL oxidation via radical-trapping abilities and act as hydrogen
donors to α-tocopherol radicals [105].

4. Antimicrobial Properties
A large amount of research has been performed assessing the antimicrobial scope of green tea
catechins. Organisms affected by green tea include a large number of Gram-positive and Gram-negative
aerobic bacteria, anaerobic bacteria, viruses, fungi, and at least one parasite (see Table 3). Among
Beverages 2017, 3, 6 7 of 14

the antimicrobial mechanisms that have been attributed to green tea are: damage to the bacterial
cell membrane, inhibition of bacterial fatty acid synthesis, inhibition of other enzymes (e.g., protein
tyrosine kinase, cysteine proteinases, DNA gyrase, ATP synthase), and inhibition of efflux pump
activity [25].
Not only do green tea catechins exhibit direct effects on microorganisms, but they also show
activities related to the prevention of infection. Studies using mice and ferrets showed that consumption
of green tea could inhibit transmission of bacteria and viruses; and studies with humans showed
that consumption of green tea resulted in fewer fever illnesses, fewer illnesses with cold or influenza
symptoms, and fewer actual infections with Influenza A or B [106].

Table 3. Organisms affected by green tea [106].

Bacteria Viruses Fungi Parasites


Acinetobacter baumannii Epstein-Barr virus Actinomyces spp. Trypanosoma cruzi
Bacillus cereus Hepatitis B Aspergillus niger
Escherichia coli (intestinal) Hepatitis C Candida albicans
Escherichia coli (uropathogenic) HIV-1
Enterococcus faecalis HSV-1
Helicobacter pylori Influenza A H1N1
Listeria monocytogenes Influenza A H3N2
Porphyromonas gingivalis Influenza A H5N2
Prevotella intermedia Influenza B
Proteus mirabilis
Pseudomonas aeruginosa
Salmonella typhi
Salmonella typhimurium
Staphylococcus aureus
Methicillin-resistant Staphylococcus aureus
Staphylococcus epidermidis
Stenotrophomonas maltophilia
Streptococcus mutans
Streptococcus pyogenes
Vibrio cholerae
Yersinia enterocolitica
Abbreviations: HIV-1, Human immunodeficiency virus-1; HSV-1, Herpes simplex virus-1.

5. Oral Health Benefits


During the course of the many research studies done using green tea catechin consumption, it was
noticed that the research subjects seemed to have improved oral health after consumption. Research
was then launched to focus on the effects of green tea on oral health. Two of the general ways in which
green tea consumption helps oral health are due to its anti-inflammatory properties, and antimicrobial
activity against mouth flora such as Streptococcus mutans [1,107,108]. The antimicrobial activity may
also be responsible for the improvement observed as to bad breath [109]. The two major types of effects
on oral health are a decrease in periodontist and dental caries.

5.1. Periodontitis
Green tea consumption has been found to result in decreased tooth loss, and prevent the
development and progression of periodontitis. Green tea consumption also has positive effects
on periodontal health when assessed as to probing depth, attachment loss, gingival bleeding, and
dentin erosion. In addition to the antimicrobial effects on the main bacteria involved in gingivitis,
Porphyromonas gingivalis, EGCG has been shown to inhibit the ability of the bacteria to bind to oral
epithelial cells via fimbriae, and has also been shown to inactivate bacterial collagenases. EGCG also
inhibits production of matrix metalloproteins and IL-8, which are responsible for initiating tissue
destruction [107,108,110,111].
Beverages 2017, 3, 6 8 of 14

5.2. Dental Caries


Prevention of dental caries is attributed to the ability of EGCG to bind and inhibit salivary and
bacterial amylases, in particular, α-amylase. EGCG also prevents generation of acid from carbohydrates
through inhibiting the transcription and function of LDH. One of the main things that encourages tooth
decay is that the major oral bacteria (e.g., Streptococcus mutans) form a biofilm on the surface of teeth.
EGCG inhibits the adherence of the bacteria to teeth, decreases biofilm formation, and inhibits the
ability of the bacteria to produce an acid environment. EGCG also inhibits the hydrogen binding and
hydrophobic interactions of bacterial collagenases. Consumption of green tea has also been associated
with an increase in oral peroxidase activity [107,111–113].

6. Conclusions
Green tea catechins have proved to be very versatile in providing health benefits. This means
that there are potential health benefits for everyone in the consumption of green tea. Even moderate
amounts of consumption (drinking 1–2 cups of tea per day) may have benefits. It is a very good thing
that it is the second most popular beverage worldwide, as the differences in health in a world without
green tea might be significant. There is fortunately a wide variety of research being performed using
green tea catechins, and we are starting to see many studies performed using human subjects, as it is
extremely important that we are able to show the direct benefits to humans. The expansive repertoire of
green tea activity in health is important, especially to those people who live where medical assistance
is not generally available or affordable.

Conflicts of Interest: The author declares no conflicts of interest.

References
1. Gupta, D.A.; Bhaskar, D.J.; Gupta, R.K.; Karim, B.; Jain, A.; Dalai, D.R. Green tea: A review on its natural
anti-oxidant therapy and cariostatic benefits. Biol. Sci. Pharm. Res. 2014, 2, 8–12.
2. Jigisha, A.; Nishant, R.; Navin, K.; Pankaj, G. Green tea: A magical herb with miraculous outcomes. Int. Res.
J. Pharm. 2012, 3, 139–148.
3. Cabrera, C.; Artacho, R.; Gimenez, R. Beneficial effects of green tea—A review. J. Am. Coll. Nutr. 2006, 25,
79–99. [CrossRef] [PubMed]
4. Botten, D.; Fugalio, G.; Fraternali, F.; Molteni, C. Structural properties of green tea catechins. J. Phys. Chem. B
2015, 119, 12860–12867. [CrossRef] [PubMed]
5. Hayat, K.; Iqbal, H.; Malik, U.; Bilal, U.; Mushtaq, S. Tea and its consumption: Benefits and risks. Crit. Rev.
Food Sci. Nutr. 2015, 55, 939–954. [CrossRef] [PubMed]
6. Wang, Y.; Ho, C.T. Polyphenolic chemistry of tea and coffee: A century of progress. J. Agric. Food Chem. 2009,
57, 8109–8114. [CrossRef] [PubMed]
7. Roowi, S.; Stalmach, A.; Mullen, W.; Lean, M.E.; Edwards, C.A.; Crozier, A. Green tea flavan-3-ols: Colonic
degradation and urinary excretion of catabolites by humans. J. Agric. Food Chem. 2010, 58, 1296–1304.
[CrossRef] [PubMed]
8. Babu, P.V.; Liu, D. Green tea catechins and cardiovascular health: An update. Curr. Med. Chem. 2008, 15,
1840–1850. [CrossRef] [PubMed]
9. Fernandez, P.L.; Pablos, F.; Martin, M.J.; Gonzalez, A.G. Study of catechin and xanthine tea profiles as
geographical tracers. J. Agric. Food Chem. 2002, 59, 1833–1839. [CrossRef]
10. Lin, Y.S.; Tsai, Y.J.; Tsay, J.S.; Lin, J.K. Factors affecting the levels of tea polyphenols and caffeine in tea leaves.
J. Agric. Food Chem. 2003, 51, 1864–1873. [CrossRef] [PubMed]
11. Liu, M.; Tian, H.I.; Wu, J.H.; Cao, R.R.; Wang, R.X.; Qi, X.H.; Xu, Q.; Chen, X.H. Relationship between gene
expression and the accumulation of catechin during spring and autumn in tea plants (Camellia sinensis L.).
Hortic. Res. 2015, 2, 15011. [CrossRef] [PubMed]
12. Lantano, C.; Rinaldi, M.; Cavazza, A.; Barbanti, D.; Corradini, C. Effects of alternative steeping methods on
composition, antioxidant property and colour of green, black and oolong tea infusions. J. Food Sci. Technol.
2015, 52, 8276–8283. [CrossRef] [PubMed]
Beverages 2017, 3, 6 9 of 14

13. Lambert, J.D.; Sang, S.; Yang, C.S. Biotransformation of green tea polyphenols and the biological activities of
those metabolites. Mol. Pharm. 2007, 4, 819–825. [CrossRef] [PubMed]
14. Henning, S.M.; Niu, Y.; Lee, N.H.; Thames, G.D.; Minutti, R.R.; Wang, H.; Go, V.L.; Heber, D. Bioavailability
and antioxidant activity of tea flavanoids after consumption of green tea, black tea, or a green tea extract
supplement. Am. J. Clin. Nutr. 2004, 80, 1558–1564. [PubMed]
15. Stalmach, A.; Troufflard, S.; Serafini, M.; Crozier, A. Absorption, metabolism and excretion of Choladi green
tea flavan-3-ols by humans. Mol. Nutr. Food Res. 2009, 53, S44–S53. [CrossRef] [PubMed]
16. Clifford, M.N.; van der Hooft, J.J.; Crozier, A. Human studies on the absorption, distribution, metabolism,
and excretion of tea polyphenols. Am. J. Clin. Nutr. 2013, 98, 1619S–1630S. [CrossRef] [PubMed]
17. Lee, M.J.; Wang, Z.Y.; Li, H.; Chen, L.; Sun, Y.; Gobbo, S.; Balentine, D.A.; Yang, C.S. Analysis of plasma and
urinary tea polyphenols in human subjects. Cancer Epidemiol. Biomark. Prev. 1995, 4, 393–399.
18. Yang, C.S.; Chen, L.; Lee, M.J.; Balentine, D.; Kuo, M.C.; Schantz, S.P. Blood and urine levels of tea catechins
after ingestion of different amounts of green tea by human volunteers. Cancer Epidemiol. Biomark. Prev. 1998,
7, 351–354.
19. Chow, H.H.; Cai, Y.; Alberts, D.S.; Hakim, I.; Dorr, R.; Shahi, F.; Crowell, J.A.; Yang, C.S.; Hara, Y. Phase I
pharmacokinetic study of tea polyphenols following single-dose administration of epigallocatechin gallate
and polyphenon E. Cancer Epidemiol. Biomark. Prev. 2001, 10, 53–58.
20. Van Amelsvoort, J.M.; Van Hof, K.H.; Mathot, J.N.; Mulder, T.P.; Wiersma, A.; Tijburg, L.B. Plasma
concentrations of individual tea catechins after a single oral dose in humans. Xenobiotica 2001, 31, 891–901.
[CrossRef] [PubMed]
21. Clarke, K.A.; Dew, T.P.; Watson, R.E.; Farrar, M.D.; Bennett, S.; Nicolaou, A.; Rhodes, L.E.; Williamson, G.
High performance liquid chromatography tandem mass spectrometry dual extraction method for
identification of green tea catechin metabolites excreted in human urine. J. Chromatogr. B Analyt. Techonol.
Biomed. Life Sci. 2014, 1, 29–37. [CrossRef] [PubMed]
22. Chow, H.H.; Cai, Y.; Hakim, I.A.; Crowell, J.A.; Shahi, F.; Brooks, C.A.; Dorr, R.T.; Hara, Y.; Alberts, D.S.
Pharmacokinetics and safety of green tea polyphenols after multiple-dose administration of epigallocatechin
gallate and polyphenon E in healthy individuals. Clin. Cancer Res. 2003, 9, 3312–3319. [PubMed]
23. Nakagawa, K.; Okuda, S.; Miyazawa, T. Dose-dependent incorporation of tea catechins, (−)-epigallocatechin-
3-gallate and (−)-epigallocatechin, into human plasma. Biosci. Biotechnol. Biochem. 1997, 61, 1981–1985.
[CrossRef] [PubMed]
24. Ullmann, U.; Haller, J.; Decourt, J.P.; Girault, N.; Girault, J.; Richard-Caudron, A.S.; Pineau, B.; Weber, P.
A single ascending dose study of epigallocatechin gallate in healthy volunteers. J. Int. Med. Res. 2003, 31,
88–101. [CrossRef] [PubMed]
25. Reygaert, W.C. The antimicrobial possibilities of green tea. Front. Microbiol. 2014, 5, 434. [CrossRef] [PubMed]
26. Shirakami, Y.; Shimizu, M.; Moriwaki, H. Cancer chemoprevention with green tea catechins: From bench to
bed. Curr. Drug Targets 2012, 13, 1842–1857. [CrossRef] [PubMed]
27. Henning, S.M.; Wang, P.; Carpenter, C.L.; Heber, D. Epigenetic effects of green tea polyphenols in cancer.
Epigenomics 2013, 5, 729–741. [CrossRef] [PubMed]
28. Subramani, C.; Natesh, R.K. Molecular mechanisms and biological implications of green tea polyphenol,
(−)-epigallocatechin-3-gallate. Int. J. Pharm. Biosci. Technol. 2013, 1, 54–63.
29. Butt, M.S.; Ahmad, R.S.; Sultan, M.T.; Qayyum, M.M.; Naz, A. Green tea and anticancer perspectives:
Updates from last decade. Crit. Rev. Food Sci. Nutr. 2015, 55, 792–805. [CrossRef] [PubMed]
30. Granja, A.; Pinheiro, M.; Reis, S. Epigallocatechin gallate nanodelivery systems for cancer therapy. Nutrients
2016, 8, E307. [CrossRef]
31. Yang, C.S.; Wang, H.; Li, G.X.; Yang, Z.; Guan, F.; Jin, H. Cancer prevention by tea: Evidence from laboratory
studies. Pharmacol. Res. 2011, 64, 113–122. [CrossRef] [PubMed]
32. Yang, C.S. Antioxidant and anti-carcinogenic activities of tea polyphenols. Arch. Toxicol. 2009, 83, 11–21.
[CrossRef] [PubMed]
33. Ju, J.; Lu, G.; Lambert, J.D.; Yang, C.S. Inhibition of carcinogenesis by tea constituents. Semin. Cancer Biol.
2007, 17, 395–402. [CrossRef] [PubMed]
34. Boehm, K.; Borelli, F.; Ernst, E.; Habacher, G.; Hung, S.K.; Milazzo, S.; Hornebar, M. Green tea
(Camellia sinensis) for the prevention of cancer. Cochrane Database Syst. Rev. 2009, 3. [CrossRef]
Beverages 2017, 3, 6 10 of 14

35. Bhoo-Pathy, N.; Peeters, P.H.; van Gils, C.; Beulens, J.W.; van der Graaf, Y.; Bueno-de-Mesquita, B.; Bulgiba, A.;
Uiterwaal, C.S. Coffee and tea intake and risk of breast. Breast Cancer Res. Treat. 2010, 121, 461–467. [CrossRef]
[PubMed]
36. Bode, A.M.; Dong, Z. Epigallocatechin 3-gallate and green tea catechins: United they work, divided they fall.
Cancer Prev. Res. (Phila.) 2009, 2, 514–517. [CrossRef] [PubMed]
37. Li, M.J.; Yin, Y.C.; Wang, J.; Jiang, Y.F. Green tea compounds in breast cancer prevention and treatment.
World J. Clin. Oncol. 2014, 5, 520–528. [CrossRef] [PubMed]
38. Umeda, D.; Yano, S.; Yamada, K.; Tachibana, H. Green tea polyphenol epigallocatechin-3-gallate signaling
pathway through 67-kDa laminin receptor. J. Biol. Chem. 2008, 283, 3050–3058. [CrossRef] [PubMed]
39. Liang, Y.C.; Lin-Shiau, S.Y.; Chen, C.F.; Lin, J.K. Inhibition of cyclin-dependent kinases 2 and 4 activities as
well as induction of Cdk inhibitors p21 and p27 during growth arrest of human breast carcinoma cells by
(−)-epigallocatechin-3-gallate. J. Cell. Biochem. 1999, 75, 1–12. [CrossRef]
40. Bain, J.; McLauchlan, H.; Elliott, M.; Cohen, P. The specificities of protein kinase inhibitors: An update.
Biochemistry 2003, 371 Pt 1, 199–204.
41. Farabegoli, F.; Papi, A.; Orlandi, M. (−)-Epigallocatechin-3-gallate down-regulates EGFR, MMP-2, MMP-9
and EMMPRIN and inhibits the invasion of MCF-7 tamoxifen-resistant cells. Biosci. Rep. 2011, 31, 99–108.
[CrossRef] [PubMed]
42. De Amicis, F.; Russo, A.; Avena, P.; Santoro, M.; Vivacqua, D.; Bonofiglio, D.; Mauro, L.; Aquila, S.;
Tramontano, D.; Fuqua, S.A.; Ando, S. In vitro mechanism for downregulation of ER-α expression by
epigallocatechin gallate in ER+/PR+ human breast cancer cells. Mol. Nutr. Food Res. 2013, 57, 840–853.
[CrossRef] [PubMed]
43. Kim, J.; Zhang, X.; Rieger-Christ, K.M.; Summerhaves, I.C.; Wazer, D.E.; Paulson, K.E.; Yee, A.S. Suppression
of Wnt signaling by the green tea compound (−)-epigallocatechin 3-gallate (EGCG) in invasive breast cancer
cells. Requirement of the transcriptional repressor HBP1. J. Biol. Chem. 2006, 281, 10865–10875. [CrossRef]
[PubMed]
44. Pianetti, S.; Guo, S.; Kavanagh, K.T.; Sonenshein, G.E. Green tea polyphenol epigallocatechin-3-gallate
inhibits Her-2/neu signaling, proliferation, and transformed phenotype of breast cancer cells. Cancer Res.
2002, 62, 652–655. [PubMed]
45. Masuda, M.; Suzui, M.; Lim, J.T.; Weinstein, I.B. Epigallocatechin-3-gallate inhibits activation of HER-2/neu
and downstream signaling pathways in human head and neck and breast carcinoma cells. Clin. Cancer Res.
2003, 9, 3486–3491. [PubMed]
46. Bigelow, R.L.; Cardelli, J.A. The green tea catechins, (−)-epigallocatechin-3-gallate (EGCG) and
(−)-epicatechin-3-gallate (ECG), inhibit HGF/Met signaling in immortalized and tumorigenic breast
epithelial cells. Oncogene 2006, 25, 1922–1930. [CrossRef] [PubMed]
47. Li, M.; He, Z.; Ermakova, S.; Zheng, D.; Tang, F.; Cho, Y.Y.; Zhu, F.; Ma, W.Y.; Sham, Y.; Rogozin, E.A.; et al.
Direct inhibition of insulin-like growth factor-I receptor kinase activity by (−)-epigallocatechin-3-gallate
regulates cell transformation. Cancer Epidemiol. Biomark. Prev. 2007, 16, 598–605. [CrossRef] [PubMed]
48. Van Aller, G.S.; Carson, J.D.; Tang, W.; Peng, H.; Zhao, L.; Copeland, R.A.; Tummino, P.J.; Luo, L.
Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR
inhibitor. Biochem. Biophys. Res. Commun. 2011, 406, 194–199. [CrossRef] [PubMed]
49. Masuda, M.; Suzui, M.; Lim, J.T.; Deguchi, A.; Soh, J.W.; Weinstein, I.B. Epigallocatechin-3-gallate decreases
VEGF production in head and neck and breast carcinoma cells by inhibiting EGFR-related pathways of
signal transduction. J. Exp. Ther. Oncol. 2002, 2, 350–359. [CrossRef] [PubMed]
50. Sartippour, M.R.; Shao, Z.M.; Heber, D.; Beatty, P.; Zhang, L.; Liu, C.; Go, V.L.; Brooks, M.N. Green tea
inhibits vascular endothelial growth factor (VEGF) induction in human breast cancer cells. J. Nutr. 2002, 132,
2307–2311. [PubMed]
51. Braicu, C.; Gherman, C.D.; Irimie, A.; Berindan-Neagoe, I. Epigallocatechin-3-gallate (EGCG) inhibits cell
proliferation and migratory behaviour of triple negative breast cancer cells. J. Nanosci. Nanotechnol. 2013, 13,
632–637. [CrossRef] [PubMed]
52. Ermakova, S.; Choi, B.Y.; Choi, H.S.; Kang, B.S.; Bode, A.M.; Dong, Z. The intermediate filament protein
vimentin is a new target for epigallocatechin gallate. J. Biol. Chem. 2005, 280, 16882–16890. [CrossRef]
[PubMed]
Beverages 2017, 3, 6 11 of 14

53. Leone, M.; Zhai, D.; Sareth, S.; Kitada, S.; Reed, J.C.; Pellecchia, M. Cancer prevention by tea polyphenols is
linked to their inhibition of antiapoptotic Bcl-2-family proteins. Cancer Res. 2003, 63, 8118–8121. [PubMed]
54. Islam, S.; Islam, N.; Kermode, T.; Johnstone, B.; Mukhtar, H.; Moskowitz, R.W.; Goldber, V.M.;
Malemud, C.J.; Haqqi, T.M. Involvement of caspase-3 in epigallocatechin-3-gallate-mediated apoptosis
of human chondrosarcoma cells. Biochem. Biophys. Res. Commun. 2000, 270, 793–797. [CrossRef] [PubMed]
55. Roy, A.M.; Baliga, M.S.; Katiyar, S.K. Epigallocatechin-3-gallate induces apoptosis in estrogen
receptor-negative human breast carcinoma cells via modulation in protein expression of p53 and Bax
and caspase-3 activation. Mol. Cancer Ther. 2005, 4, 81–90. [PubMed]
56. Alshatwi, A.A. Catechin hydrate suppresses MCF-7 proliferation through TP53/Caspase-mediated apoptosis.
J. Exp. Clin. Cancer Res. 2010, 29, 167. [CrossRef] [PubMed]
57. Ermakova, S.P.; Kang, B.S.; Choi, B.Y.; Choi, H.S.; Schuster, T.F.; Ma, W.Y.; Bode, A.M.; Dong, Z.
(−)-Epigallocatechin gallate overcomes resistance to etoposide-induced cell death by targeting the molecular
chaperone glucose-regulated protein 78. Cancer Res. 2006, 66, 9260–9269. [CrossRef] [PubMed]
58. Jochmann, N.; Baumann, G.; Stangl, V. Green tea and cardiovascular disease: From molecular targets towards
human health. Curr. Opin. Clin. Nutr. Metab. Care 2008, 11, 758–765. [CrossRef] [PubMed]
59. Nakachi, K.; Matsuyama, S.; Miyake, S.; Suganuma, M.; Imai, K. Preventive effects of drinking green tea on
cancer and cardiovascular disease: Epidemiological evidence for multiple targeting prevention. Biofactors
2000, 13, 49–54. [CrossRef] [PubMed]
60. Kuriyama, S.; Shimazu, T.; Ohmori, K.; Kikuchi, N.; Nakaya, N.; Nishino, Y.; Tsubono, Y.; Tsuji, I. Green tea
consumption and mortality due to cardiovascular disease, cancer, and all causes in Japan: The Ohsaki study.
JAMA 2006, 296, 1255–1265. [CrossRef] [PubMed]
61. Nagao, T.; Hase, T.; Tokimitsu, I. A green tea extract high in catechins reduces body fat and cardiovascular
risks in humans. Obesity (Silver Spring) 2007, 15, 1473–1483. [CrossRef] [PubMed]
62. Fukino, Y.; Shimbo, M.; Aoki, N.; Okubo, T.; Iso, H. Randomized controlled trial for an effect of green
tea consumption on insulin resistance and inflammation markers. J. Nutr. Sci. Vitaminol. (Tokyo) 2005, 51,
335–342. [CrossRef] [PubMed]
63. Peters, U.; Poole, C.; Arab, L. Does tea affect cardiovascular disease? A meta-analysis. Am. J. Epidemiol. 2001,
154, 495–503. [CrossRef] [PubMed]
64. Mukamal, K.J.; Maclure, M.; Muller, J.E.; Sherwood, J.B.; Mittleman, M.A. Tea consumption and mortality
after acute myocardial infarction. Circulation 2002, 105, 2476–2481. [CrossRef] [PubMed]
65. Widlanski, M.E.; Hamburg, N.M.; Anter, E.; Holbrook, M.; Kahn, D.F.; Elliott, J.G.; Keaney, J.F., Jr.; Vita, J.A.
Acute EGCG supplementation reverses endothelial dysfunction in patients with coronary artery disease.
J. Am. Coll. Nutr. 2007, 26, 95–102. [CrossRef]
66. Ponzo, V.; Goitre, I.; Fadda, M.; Gambino, R.; De Francesco, A.; Soldati, L.; Gentile, L.; Magistroni, P.;
Cassader, M.; Bo, S. Dietary flavonoid intake and cardiovascular risk: A population-based cohort study.
J. Transl. Med. 2015, 13, 218. [CrossRef] [PubMed]
67. Serafini, M.; Del Rio, D.; Yao, D.N.; Bettuzzi, S.; Peluso, I. Chapter 12: Health benefits of tea. In Herbal Medicine:
Biomolecular, and Clinical Aspects, 2nd ed.; Benzie, I.F.F., Wachtel-Galor, S., Eds.; CRC Press: Boca Raton, FL,
USA, 2011; pp. 239–262.
68. Ahmed, S.; Marotte, H.; Kwan, K.; Ruth, J.H.; Campbell, P.L.; Rabquer, B.J.; Pakozdi, A.; Koch, A.E.
Epigallocaetchin-3-gallate inhibits IL-6 synthesis and suppresses transsignaling by enhancing soluble gp130
production. Proc. Natl. Acad. Sci. USA 2008, 105, 14692–14697. [CrossRef] [PubMed]
69. Yun, H.J.; Yoo, W.H.; Han, M.K.; Lee, Y.R.; Kim, J.S.; Lee, S.I. Epigallocatechin-3-gallate suppresses
TNF-α-induced production of MMP-1 and -3 in rheumatoid arthritis synovial fibroblasts. Rheumatol. Int.
2008, 29, 23–29. [CrossRef] [PubMed]
70. Leong, D.J.; Choudhury, M.; Hanstein, R.; Hirsh, D.M.; Kim, S.J.; Majeska, R.J.; Schaffler, M.B.; Hardin, J.A.;
Spray, D.C.; Goldring, M.B.; et al. Green tea polyphenol treatment is chondroprotective, anti-inflammatory
and palliative in a mouse posttraumatic osteoarthritis model. Arthritis Res. Ther. 2014, 16, 508. [CrossRef]
[PubMed]
71. Naito, Y.; Yoshikawa, T. Green tea and heart health. J. Cardiovasc. Pharmacol. 2009, 54, 385–390. [CrossRef]
[PubMed]
Beverages 2017, 3, 6 12 of 14

72. Liu, D.; Perkins, J.T.; Hennig, B. EGCG prevents PCB-126-induced endothelial cell inflammation via
epigenetic modifications of NF-κB target genes in human endothelial cells. J. Nutr. Biochem. 2016, 28,
164–170. [CrossRef] [PubMed]
73. Donà, M.; Dell’Aica, I.; Calabrese, F.; Benelli, R.; Morini, M.; Albini, A.; Garbisa, S. Neutrophil restraint by
green tea: Inhibition of inflammation, associated angiogenesis, and pulmonary fibrosis. J. Immunol. 2003,
170, 4335–4341. [CrossRef] [PubMed]
74. Akhtar, N.; Haqqi, T.M. Epigallocatechin-3-gallate suppresses the global interleukin-1beta-induced
inflammatory response in human chondrocytes. Arthritis Res. Ther. 2011, 13, r93. [CrossRef] [PubMed]
75. Behfarnia, P.; Aslani, A.; Jamshidian, F.; Noohi, S. The efficacy of green tea chewing gum on gingival
inflammation. J. Dent. Shiraz Univ. Med. Sci. 2016, 17, 149–154.
76. Kim, I.B.; Kim, D.Y.; Lee, S.J.; Sun, M.J.; Lee, M.S.; Li, H.; Cho, J.J.; Park, C.S. Inhibition of IL-8 production
by green tea polyphenols in human nasal fibroblasts and A549 epithelial cells. Biol. Pharm Bull. 2006, 29,
1120–1125. [CrossRef] [PubMed]
77. Tang, Y.; Matsuoka, I.; Ono, T.; Inoue, K.; Kimura, J. Selective up-regulation of P2X4 -receptor gene expression
by interferon-γ in vascular endothelial cells. J. Pharmacol. Sci. 2008, 107, 419–427. [CrossRef] [PubMed]
78. Liu, X.; Zhang, D.Y.; Zhang, W.; Zhao, X.; Yuan, C.; Ye, F. The effect of green tea extract and EGCG on the
signaling network in squamous cell carcinoma. Nutr. Cancer 2011, 63, 466–475. [CrossRef] [PubMed]
79. Baba, Y.; Sonoda, J.I.; Hayashi, S.; Tosuji, N.; Sonoda, S.; Makisumi, K.; Nakajo, M. Reduction of oxidative
stress in liver cancer patients by oral green tea polyphenol tablets during hepatic arterial infusion
chemotherapy. Exp. Ther. Med. 2012, 4, 452–458. [CrossRef] [PubMed]
80. Tao, L.; Forester, S.C.; Lambert, J.D. The role of the mitochondrial oxidative stress in the cytotoxic effects of
the green tea catechin, (−)-epigallocatechin-3-gallate, in oral cells. Mol. Nutr. Food Res. 2014, 58, 665–676.
[CrossRef] [PubMed]
81. Calo, L.A.; Vertolli, U.; Davis, P.A.; Dal Maso, L.; Pagnin, E.; Ravarotto, V.; Maiolino, G.; Lupia, M.;
Seccia, T.M.; Rossi, G.P. Molecular biology based assessment of green tea effects on oxidative stress and
cardiac remodeling in dialysis patients. Clin. Nutr. 2014, 33, 437–442. [CrossRef] [PubMed]
82. Vester, H.; Holzer, N.; Neumaier, M.; Lilianna, S.; Nüssler, A.K.; Seeliger, C. Green tea extract (GTE) improves
differentiation in human osteoblasts during oxidative stress. J. Inflamm. (Lond.) 2014, 11, 15. [CrossRef]
[PubMed]
83. Sugita, M.; Kapoor, M.P.; Nishimura, A.; Okubo, T. Influence of green tea catechins on oxidative stress
metabolites at rest and during exercise in healthy humans. Nutrition 2016, 32, 321–331. [CrossRef] [PubMed]
84. Jówko, E.; Sacharuk, J.; Balasinska, B.; Wilczak, J.; Charmas, M.; Ostraszewski, P.; Charmas, R. Effect of a
single dose of green tea polyphenols on the blood markers of exercise-induced oxidative stress in soccer
players. Int. J. Sport Nutr. Exerc. Metab. 2012, 22, 486–496. [CrossRef] [PubMed]
85. Zhao, J.; Fang, S.; Yuan, Y.; Guo, Z.; Zeng, J.; Guo, Y.; Tang, P.; Mei, X. Green tea polyphenols protect spinal
cord neurons against hydrogen peroxide-induced oxidative stress. Neural Regen. Res. 2014, 9, 1379–1385.
[PubMed]
86. Jówko, E.; Długoł˛ecka, B.; Makaruk, B.; Cieśliński, I. The effect of green tea extract supplements on
exercise-induced oxidative stress parameters in male sprinters. Eur. J. Nutr. 2015, 54, 783–791. [CrossRef]
[PubMed]
87. Bogdanski, P.; Suliburska, J.; Szulinska, M.; Stepien, M.; Pupek-Musialik, D.; Jablecka, A. Green tea extract
reduces blood pressure, inflammatory biomarkers, and oxidative stress and improves parameters associated
with insulin resistance in obese, hypertensive patients. Nutr. Res. 2012, 32, 421–427. [CrossRef] [PubMed]
88. Li, M.; Liu, J.T.; Pang, X.M.; Han, C.J.; Mao, J.J. Epigallocatechin-3-gallate inhibits angiotensin II and
interleukin-6-induced C-reactive protein production in macrophages. Pharmacol. Rep. 2012, 64, 912–918.
[CrossRef]
89. Bhardwaj, P.; Khanna, D. Green tea catechins: Defensive role in cardiovascular disorders. Chin. J. Nat. Med.
2013, 11, 345–353. [CrossRef]
90. Son, D.J.; Cho, M.R.; Jin, Y.R.; Kim, S.Y.; Park, Y.H.; Lee, S.H.; Akiba, S.; Sato, T.; Yun, Y.P. Antiplatelet effect of
green tea catechins: A possible mechanism through arachidonic acid pathway. Prostaglandins Leukot. Essent.
Fatty Acids 2004, 71, 25–31. [CrossRef] [PubMed]
Beverages 2017, 3, 6 13 of 14

91. Jin, Y.R.; Im, J.H.; Park, E.S.; Cho, M.R.; Han, X.H.; Lee, J.J.; Lim, Y.; Kim, T.J.; Yun, Y.P. Antiplatelet activity
of epigallocatechin gallate is mediated by the inhibition of PLCγ2 phosphorylation, elevation of PGD2
production, and maintaining calcium-ATPase activity. J. Cardiovasc. Pharmacol. 2008, 51, 45–54. [CrossRef]
[PubMed]
92. Ok, W.J.; Cho, H.J.; Kim, H.H.; Lee, D.H.; Kang, H.Y.; Kwon, H.W.; Rhee, M.H.; Kim, M.; Park, H.J.
Epigallocatechin-3-gallate has an anti-platelet effect in a cyclic AMP-dependent manner. J. Atheroscler.
Thromb. 2012, 19, 337–348. [CrossRef] [PubMed]
93. Lee, D.H.; Kim, Y.J.; Kim, H.H.; Cho, H.J.; Ryu, J.H.; Rhee, M.H.; Park, H.J. Inhibitory effects of
epigallocatechin-3-gallate on microsomal cyclooxygenase-1 activity in platelets. Biomol. Ther. 2013, 21,
54–59. [CrossRef] [PubMed]
94. Iida, Y.; Doi, T.; Matsushima-Nishiwaki, R.; Tokuda, H.; Ogura, S.; Kozawa, O.; Iida, H. (−)-Epigallocatechin
gallate selectively inhibits adenosine diphosphate-stimulated human platelet activation: Suppression of
heat shock protein 27 phosphorylation via p38 mitogen-activated protein kinase. Mol. Med. Rep. 2014, 10,
1383–1388. [CrossRef] [PubMed]
95. Jain, K.S.; Kathiravan, M.K.; Somani, R.S.; Shisloo, C.J. The biology and chemistry of hyperlipidemia.
Bioorg. Med. Chem. 2007, 15, 4674–4699. [CrossRef] [PubMed]
96. Parthasarathy, S.; Raghavamenon, A.; Gareinabi, M.O.; Santanam, N. Oxidized low-density lipoprotein.
Methods Mol. Biol. 2010, 610, 403–417. [PubMed]
97. Kim, A.; Chiu, A.; Barone, M.K.; Avino, D.; Wang, F.; Coleman, C.I.; Phung, O.J. Green tea catechins decrease
total and low-density lipoprotein cholesterol: A systematic review and meta-analysis. J. Am. Diet. Assoc.
2011, 111, 1720–1729. [CrossRef] [PubMed]
98. Zheng, X.X.; Xu, Y.L.; Li, S.H.; Liu, X.X.; Hui, R.; Huang, X.H. green tea intake lowers fasting serum total and
LDL cholesterol in adults: A meta-analysis of 14 randomized controlled trials. Am. J. Clin. Nutr. 2011, 94,
601–610. [CrossRef] [PubMed]
99. Wu, A.H.; Spicer, D.; Stanczyk, F.Z.; Tseng, C.C.; Yang, C.S.; Pike, M.C. Effect of 2 month controlled green tea
intervention on lipoprotein cholesterol, glucose, and hormone levels in healthy postmenopausal women.
Cancer Prev. Res. (Phila.) 2012, 5, 393–402. [CrossRef] [PubMed]
100. Khalesi, S.; Sun, J.; Buys, N.; Jamashidi, A.; Nikbakht-Nasrabadi, E.; Khosravi-Boroujeni, H. Green tea
catechins and blood pressure: A systematic review and meta-analysis of randomized controlled trials.
Eur. J. Nutr. 2014, 53, 1299–1311. [CrossRef] [PubMed]
101. Ohmori, R.; Kondo, K.; Momiyama, Y. Antioxidant beverages: Green tea intake and coronary artery disease.
Clin. Med. Insights Cardiol. 2014, 8 (Suppl. 3), 7–11. [CrossRef] [PubMed]
102. Onakpoya, I.; Spencer, E.; Heneghan, C.; Thompson, M. The effect of green tea on blood pressure and lipid
profile: A systematic review and meta-analysis of randomized clinical trials. Nutr. Met. Cardiovasc. Dis. 2014,
24, 823–836. [CrossRef] [PubMed]
103. Takechi, R.; Alfonso, H.; Hiramatsu, N.; Ishisaka, A.; Tanaka, A.; Tan, L.B.; Lee, A.H. Elevated plasma and
urinary concentrations of green tea catechins associated with improved plasma lipid profile in healthy
Japanese women. Nutr. Res. 2016, 36, 220–226. [CrossRef] [PubMed]
104. Tian, C.; Huang, Q.; Yang, L.; Légaré, S.; Angileri, F.; Yang, H. Green tea consumption is associated with
reduced incident CHD and improved CHD-related biomarkers in the Dongfeng-Tongji cohort. Sci. Rep.
2016, 6, 24353. [CrossRef] [PubMed]
105. Suzuki-Sugihara, N.; Kishimoto, Y.; Saita, E.; Taguchi, C.; Kobayashi, M.; Ichitani, M.; Ukawa, Y.;
Sagesaka, Y.M.; Suzuki, E.; Kondo, K. Green tea catechins prevent low-density lipoprotein oxidation via
their accumulation in low-density lipoprotein particles in humans. Nutr. Res. 2016, 36, 16–23. [CrossRef]
[PubMed]
106. Reygaert, W.C. Potential for Prevention of Infection by Green Tea. In Green Tea and Health: Antioxidant
Properties, Consumption and Role in Disease Prevention; Powell, N., Ed.; Nova Science Pub Inc.: Hauppauge,
NY, USA, 2015.
107. Gaur, S.; Agnihotri, R. Green tea: A novel functional food for the oral health of older adults.
Geriatr. Gerontol. Int. 2014, 14, 238–250. [CrossRef] [PubMed]
108. Awadalla, H.I.; Ragab, M.H.; Bassuoni, M.W.; Fayed, M.T.; Abbas, M.O. A pilot study of the role of green tea
use on oral health. Int. J. Dent. Hyg. 2011, 9, 110–116. [CrossRef] [PubMed]
Beverages 2017, 3, 6 14 of 14

109. Rassameemasmaung, S.; Phusudsawang, P.; Sangalungkarn, V. Effect of green tea mouthwash on oral
malodor. ISRN Prev. Med. 2012, 2013, 975148. [CrossRef] [PubMed]
110. Kushiyama, M.; Shimazaki, Y.; Murakami, M.; Yamashita, Y. Relationship between intake of green tea and
periodontal disease. J. Periodontol. 2009, 80, 372–377. [CrossRef] [PubMed]
111. Kato, M.T.; Magalháes, A.C.; Rios, D.; Hannas, A.R.; Attin, T.; Buzalaf, M.A. Protective effect of green tea on
dentin erosion and abrasion. J. Appl. Oral Sci. 2009, 17, 560–564. [CrossRef] [PubMed]
112. Hara, K.; Ohara, M.; Hayashi, I.; Hino, T.; Nishimura, R.; Iwasaki, Y.; Ogawa, T.; Ohyama, Y.; Sugiyama, M.;
Amano, H. The green tea polyphenol (−)-epigallocatechin gallate precipitates salivary proteins including
alpha-amylase: Biochemical implications for oral health. Eur. J. Oral Sci. 2012, 120, 132–139. [CrossRef]
[PubMed]
113. Narotzki, B.; Levy, Y.; Aizenbud, D.; Reznick, A.Z. Green tea and its major polyphenol EGCG increase the
activity of oral peroxidases. Adv. Exp. Med. Biol. 2013, 756, 99–104. [PubMed]

© 2017 by the author; licensee MDPI, Basel, Switzerland. This article is an open access
article distributed under the terms and conditions of the Creative Commons Attribution
(CC-BY) license (http://creativecommons.org/licenses/by/4.0/).

You might also like