PROTECTION AGAINST ULTRAVIOLET‐B RADIATION‐INDUCED LOCAL and SYSTEMIC SUPPRESSION OF CONTACT HYPERSENSITIVITY and EDEMA RESPONSES IN C3H/HeN MICE BY GREEN TEA POLYPHENOLS
- 1 November 1995
- journal article
- Published by Wiley in Photochemistry and Photobiology
- Vol. 62 (5) , 855-861
- https://doi.org/10.1111/j.1751-1097.1995.tb09147.x
Abstract
— Exposure of skin to UV radiation can cause diverse biological effects, including induction of inflammation, alteration in cutaneous immune cells and impairment of contact hypersensitivity (CHS) responses. Our laboratory has demonstrated that oral feeding as well as topical application of a poly-phenolic fraction isolated from green tea (GTP) affords protection against the carcinogenic effects of UVB (280–320 nm) radiation. In this study, we investigated whether GTP could protect against UVB-induced immunosuppression and cutaneous inflammatory responses in C3H mice. Immunosuppression was assessed by contact sensitization with 2,4-dinitrofluorobenzene applied to UVB-irradiated skin (local suppression) or to a distant site (systemic suppression), while double skin-fold swelling was used as the measure of UVB-induced inflammation. Topical application of GTP (1–6 mg/animal), 30 min prior to or 30 min after exposure to a single dose of UVB (2 kj/m2) resulted in significant protection against local (25–90%) and systemic suppression (23–95%) of CHS and inflammation in mouse dorsal skin (70–80%). These protective effects were dependent on the dose of GTP employed; increasing the dose (1–6 mg/animal) resulted in an increased protective effect (25–93%). The protective effects were also dependent on the dose of UVB (2–32 kJ/m2). Among the four major epicatechin derivatives present in GTP, (-)-epigallocatechin-3-gallate, the major constituent in GTP, was found to be the most effective in affording protection against UVB-caused CHS and inflammatory responses. Our study suggests that green tea, specifically polyphenols present therein, may be useful against inflammatory dermatoses and immunosuppression caused by solar radiation.Keywords
This publication has 37 references indexed in Scilit:
- Leukotrienes as mediators of skin inflammationBritish Journal of Dermatology, 2006
- Effect of Ultraviolet Radiation on Cataract FormationNew England Journal of Medicine, 1988
- Multiple Topical Applications of Arachidonic Acid to Mouse Ears Induce Inflammatory and Proliferative ChangesJournal of Investigative Dermatology, 1988
- Arachidonic acid metabolism by isolated epidermal basal and differentiated keratinocytes from the hairless mouseBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, 1986
- Prostaglandins in human skin diseaseBritish Journal of Dermatology, 1983
- Arachidonic acid metabolism in guinea pig skinBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, 1982
- SUPPRESSION OF CONTACT HYPERSENSITIVITY BY UV RADIATION AND ITS RELATIONSHIP TO UV-INDUCED SUPPRESSION OF TUMOR IMMUNITYPhotochemistry and Photobiology, 1981
- SUPPRESSION OF CONTACT HYPERSENSITIVITY BY UV RADIATION AND ITS RELATIONSHIP TO UV-INDUCED SUPPRESSION OF TUMOR IMMUNITYPhotochemistry and Photobiology, 1981
- Ultraviolet light treatment delays contact sensitization to nitrogen mustardBritish Journal of Dermatology, 1981
- Sunscreens prevent ultraviolet photocarcinogenesisJournal of the American Academy of Dermatology, 1980