Role of Green Tea in Reducing Epidermal Thickness upon Ultraviolet Light-B Injury in BALB/c Mice (original) (raw)
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Photochemistry and Photobiology, 1993
In prior studies we and others have shown that oral feeding of a polyphenolic fraction isolated from green tea (GTP) or water extract of green tea affords protection against ultraviolet B (UVB) radiation-induced carcinogenesis in SKH-I hairless mice (Wang et al., Carcinogenesis 12, 1527-1 530, 1991. It is known that exposure of murine skin to UVB radiation results in cutaneous edema, depletion of the antioxidant-defense system and induction of ornithine decarboxylase (ODC) and cyclooxygenase activities. In this study we assessed the protective effect of GTP on these UVB radiation-caused changes in murine skin. Oral feeding of 0.2% GTP (wtlvol) as the sole source of drinking water for 30 days to SKH-I hairless mice followed by irradiation with UVB (900 mJ/cm2) resulted in significant protection against UVB radiation-caused cutaneous edema (P < 0.0005) and depletion of the antioxidant-defense system in epidermis ( P < 0.01-0.02). The oral feeding of GTP also resulted in significant protection against UVB radiation-caused induction of epidermal ODC ( P < 0.005-0.01) and cyclooxygenase activities (P < 0.0001) in a time-dependent manner. Our data indicate that the inhibition of UVB radiation-caused changes in these markers of tumor promotion in murine skin by GTP may be one ofthe possible mechanisms ofchemopreventive effectsassociated with green tea against UVB-induced tumorigenesis. The results of this study suggest that green tea, specifically polyphenols present therein, may be useful against inflammatory responses associated with the exposure of skin to solar radiation.
The American journal of clinical nutrition, 2015
Safe systemic protection from the health hazards of ultraviolet radiation (UVR) in sunlight is desirable. Green tea is consumed globally and is reported to have anti-inflammatory properties, which may be mediated through the impact on cyclooxygenase and lipoxygenase pathways. Recent data suggest that green tea catechins (GTCs) reduce acute UVR effects, but human trials examining their photoprotective potential are scarce. We performed a double-blind, randomized, placebo-controlled trial to examine whether GTCs protect against clinical, histologic, and biochemical indicators of UVR-induced inflammation. Healthy adults (aged 18-65 y, phototypes I-II) were randomly allocated to 1350 mg encapsulated green tea extract (540 mg GTC) with 50 mg vitamin C or placebo twice daily for 3 mo. Impact on skin erythema, dermal leukocytic infiltration, and concentrations of proinflammatory eicosanoids was assessed after solar-simulated UVR challenge, and subject compliance was determined through assa...
Photoprotective Effect of Black Tea Extracts Against UVB-induced Phototoxicity in Skin
Photochemistry and Photobiology, 1999
Ultraviolet (UV) exposure induces photodamage of skin. It is a matter of concern that the level of UV radiation reaching the earth surface is increasing as a result of depletion of the stratospheric ozone, and climate change. It is urgently necessary to develop strategies to protect the skin from UV-induced injuries. Tea extracts are gaining increasing attention as a supplement in skin care products. However, the factors contributing to the photoprotective effects of tea extracts have not been systematically defined and conflicting results about the effect of tea extracts on photodamage have been reported. In this paper, the literature dealing with the use of tea and its extracts for the prevention of photodamage to the skin as well as the photoprotective effects of tea and its extracts have been highlighted. The potential chemopreventive agents in tea include catechins, caffeine, polysaccharides, apigenin and luteolin which inhibit, reverse or retard the process of the skin photodamage via their sunscreen and antioxidant properties, regulation of signal transduction pathway and gene expression, alleviation of DNA damage, and modulation immunological function are also presented. Existing gaps in this research field include incomplete clarity of photochemopreventive mechanism of tea, the adverse or side effects of tea extracts owing to residues or impurity and the instability of the functional components of tea during storage.
Photochemistry and Photobiology, 1999
Identification of natural products capable of affording protection against UVB radiation-induced inflammatory responses and generation of oxidative stress may have important human health implications. The UVB exposure-induced skin injury and oxidative stress has been associated with a variety of skin disease conditions including photoaging, inflammation and cancer. Tea is a popular beverage consumed worldwide. In several mouse skin models, topical application as well as oral consumption of green tea has been shown to afford protection against chemical and UVB-induced carcinogenesis and inflammatory responses. In the present study, we investigated in human skin, whether topical application of (-)epigallocatechin-3-gallate (EGCG), the major polyphenolic constituent in green tea, inhibits UVB-induced infiltration of leukocytes (macrophageheutrophils), a potential source of generation of reactive oxygen species (ROS), and generation of prostaglandin (PG) metabolites. Human subjects were UVB irradiated on sun-protected skin to four times their minimal erythema dosage (MED) and skin biopsies or keratomes were obtained either 24 h or 48 h later. We found that topical application of EGCG (3 md2.5 cm') before UVB (4 MED) exposure to human skin significantly blocked UVB-induced infiltration of leukocytes and reduced myeloperoxidase activity. These infiltrating leukocytes are considered to be the major source of generation of ROS. In the same set of experiments we found that topical application of EGCG before UVB exposure decreased UVB-induced erythema.
Green Tea Protects Against Psoralen Plus Ultraviolet A-Induced Photochemical Damage to Skin1
Journal of Investigative Dermatology, 1999
The use of psoralens combined with exposure to ultraviolet A radiation is a major form of treatment for psoriasis and a number of other common skin diseases. Although psoralen plus ultraviolet A treatment is highly effective, careful follow-up cohort studies have shown that it greatly increases risk for the development of cutaneous squamous cell carcinoma and melanoma. Strategies to reduce the risk of cancer development in psoralen plus ultraviolet A-treated populations are highly desirable. In prior studies, we demonstrated that green tea and constituent polyphenols protect against ultraviolet Binduced carcinogenesis and reduce the growth rate of established tumors in skin. In this study, we show that pre-and post-treatment with standardized green tea extract in psoralen plus ultraviolet A treatment populations abrogates the psoralen plus ultraviolet A-induced photochemical damage to skin. Intact mouse and human skin and reconstituted human skin were employed to assess the effect of both topical and oral administration of standardized green tea extract against psoralen plus ultraviolet Ainduced photodamage. Oral administration of standardized green tea extract prior to and during multiple psoralen plus ultraviolet A treatments reduced hyperplasia and hyperkeratosis in murine skin. Standardized green tea extract treatment also inhibited accumulation of c-fos and p53 protein induction following a single exposure to psoralen plus ultraviolet A. c-fos and p53 positive cells in psoralen plus ultraviolet A-treated skin were found to be increased by 55.4 6 13.6% and 62.3 6 10.5%, respectively, compared with saline-treated unexposed control skin. Oral administration of 0.4 or 0.8% standardized green tea extract inhibited c-fos protein accumulation by 18.5% and 46.2% (p < 0.05), respectively, and p53 protein accumulation by 26.1% and 54.3% (p < 0.05), respectively. Similarly proliferating cell nuclear antigen staining, a marker of cell proliferation was induced (73.7%) in psoralen plus ultraviolet A-treated skin. Oral administration of 0.4% or 0.8% standardized green tea extract 1 d after psoralen plus ultraviolet A treatment was effective in reducing psoralen plus ultraviolet A-induced in¯ammatory responses including erythema and edema formation. When standardized green tea extract was applied to EpiDerm, a reconstituted human skin equivalent, psoralen plus ultraviolet A-induced 8-methoxypsoralen-DNA adduct formation and p53 protein accumulation were inhibited. Topical application of 0.2 mg 8-methoxypsoralen per cm 2 followed by exposure to ultraviolet A (2.5 J per cm 2 ) resulted in delayed erythema formation in human subjects. Pretreatment of human skin with topical application of 0.2 mg standardized green tea extract per cm 2 30 min prior to psoralen plus ultraviolet A treatment resulted in an almost complete abrogation of psoralen plus ultraviolet A-induced erythema. In summary, these data demonstrate that standardized green tea extract protects against psoralen plus ultraviolet A-induced phototoxicity by inhibiting DNA damage and diminishing the in¯ammatory effects of this modality.
Effects of polyphenols on skin damage due to ultraviolet A rays: an experimental study on rats
Journal of The European Academy of Dermatology and Venereology, 2007
Background Ultraviolet (UV) radiation causes many acute and chronic conditions such as oedema of the skin, sunburn, immunosuppression, photoageing and skin cancer. The use of antioxidants has become of paramount importance in prevention of the damage caused by ultraviolet radiation. Epigallocatechin-3-gallate (EGCG), one of the main components of green tea, has been reported to have anti-inflammatory, antioxidant and anticarcinogenic properties. Aim The aim of this experimental study was to investigate to what extent EGCG prevented acute skin damage caused by UVA. Material and method The sample contained 2% EGCG, which was prepared in hydrophilic ointment (USP XXIV) as the vehicle. Twenty-four 12-week-old Wistar albino rats are included in the study and divided into four groups, each containing six rats. Group I was formed to be the control group, which was not applied any topical medication or exposed to UV radiation. Group II was formed to observe acute effects of UVA on the skin, Group III was formed to observe effectiveness of topical EGCG on the skin applied 30 min after exposure to UVA, and Group IV was formed to observe topical EGCG applied 30 min before exposure to UVA. All groups were examined for sunburn cells, leucocyte infiltration, dermo-epidermal activity, collagen changes and elastic fibre pathologies on 24 and 72 h. Statistical analysis was performed using SPSS 11.5, and chi-squared test was used for the evaluation of parameters. Results Group IV showed a statistically significant decrease in sunburn cells and dermo-epidermal activation compared with Group II. Group II showed significant increase in all parameters compared with Group I, showing the effects of UV exposure alone, and no difference was detected in Group II and III. Conclusion These results show a protective effect of EGCG when applied topically before UVA exposure. No benefit was detected when EGCG was applied after UV exposure.
Molecules, 2007
Epicatechin-3-gallate (ECG) is a polyphenolic compound similar to (-)-epigallocatechin-3-gallate (EGCG) which is abundant in green tea. Numerous workers have proposed that EGCG protects epidermal cells against UVB-induced damage. However, little has been known about whether ECG protects keratinocytes against UVB-induced damage. We decided to investigate the protective effects and underlying mechanisms of ECG on UVB-induced damage. Cell viability was determined by the MTT assay. Activation of ERK1/2, p38 and JNK was analyzed by Western blotting. Intracellular H 2 O 2 production and DNA content was analyzed by flow cytometry. Lipid peroxidation was assayed by colorimetry. In our study, we found that ECG dose-dependently attenuated UVB-induced keratinocyte death. Moreover, ECG markedly inhibited UVB-induced cell membrane lipid peroxidation and H 2 O 2 generation in keratinocytes, suggesting that ECG can act as a free radical scavenger when keratinocytes were photodamaged. In parallel, H 2 O 2 -induced the activation of ERK1/2, p38 and JNK in keratinocytes could be inhibited by ECG. UVB-induced pre-G 1 arrest leading to apoptotic changes of keratinocytes were blocked by ECG. Taken together, we provide here evidence that ECG protects keratinocytes from Molecules 2007, 12 1846 UVB-induced photodamage and H 2 O 2 -induced oxidative stress, possibly through inhibition of the activation of ERK1/2, p38 and JNK and/or scavenging of free radicals.
Cancer Research, 1992
Green tea was prepared by extracting 12.5 g of green tea leaves twice with 500 ml of boiling water, and the extracts were combined. This 1.25% green tea extract (1.25 g of tea leaves/100 ml of water) contained 4.69 mg of green tea extract solids per ml and was similar in composition to some green tea beverages consumed by humans. A 2.5% green tea extract (2.5 g of tea leaves/100 ml of water) was prepared similarly. Treatment of female SKH-1 mice with 180 m.l/rnr of ultraviolet B light (UVB) once daily for 7 days resulted in red sunburn lesions of the skin. The intensity of red color and area of these lesions were inhibited in a dosedependent fashion by the administration of 1.25 or 2.5% green tea extract as the sole source of drinking water before and during UVB treatment. Treatment of female SKH-1 mice with 180 in.I/cnr of UVB once daily for 10 days followed 1 wk later by twice weekly application of 12-0tetradecanoylphorbol-13-acetate for 25 wk resulted in the development of skin tumors. The formation of skin tumors was inhibited by adminis tration of 1.25% green tea extract as the sole source of drinking water prior to and during the 10 days of UVB treatment and for 1 wk after UVB treatment. In additional experiments, female SKH-1 mice were treated with 200 nmol of 7,12-dimethylbenz(a)anthracene followed 3 wk later by irradiation with 180, 60, or 30 mj/cm2 of UVB twice weekly for 30 wk. UVB-induced formation of skin tumors and increased spleen size were inhibited by administration of 1.25% green tea extract as the sole source of drinking water prior to and during the 30 wk of UVB treatment. In these experiments, treatment of the animals with the green tea extract not only decreased the number of skin tumors but also decreased sub stantially the size of the tumors. In additional studies, SKH-1 mice were initiated by topical application of 200 nmol of 7,12-dimethylbenz(a)anthracene followed by twice weekly application of 12-0-tetradecanoylphorbol-13-acetate for 25 wk. Administration of 1.25% green tea extract as the sole source of drinking water during promotion with 12-0-tetradecanoylphorbol-13-acetate reduced the number and incidence of skin tumors.