Green tea polyphenols: DNA photodamage and photoimmunology

被引:70
作者
Katiyar, SK [1 ]
Bergamo, BM [1 ]
Vyalil, PK [1 ]
Elmets, CA [1 ]
机构
[1] Univ Alabama, Sch Med, Dept Dermatol, Birmingham, AL 35294 USA
关键词
green tea polyphenols; (-)-epigallocatechin-3-gallate; ultraviolet light; photoimmunology; DNA photodamage;
D O I
10.1016/S1011-1344(01)00248-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Green tea is a popular beverage consumed worldwide. The epicatechin derivatives, which are commonly called `polyphenols', are the active ingredients in green tea and possess antioxidant, anti-inflammatory and anti-carcinogenic properties. Studies conducted by our group on human skin have demonstrated that green tea polyphenols (GTP) prevent ultraviolet (UV)-B-induced cyclobutane pyrimidine dimers (CPD), which are considered to be mediators of UVB-induced immune suppression and skin cancer induction. GTP treated human skin prevented penetration of UV radiation, which was demonstrated by the absence of immunostaining for CPD in the reticular dermis. The topical application of GTP or its most potent chemopreventive constituent (-)-epigallocatechin-3-gallate (EGCG) prior to exposure to UVB protects against UVB-induced local as well as systemic immune suppression in laboratory animals. Additionally, studies have shown that EGCG treatment of mouse skin inhibits UVB-induced infiltration of CD11b+ cells. CD11b is a cell surface marker for activated macrophages and neutrophils, which are associated with induction of UVB-induced suppression of contact hypersensitivity responses. EGCG treatment also results in reduction of the UVB-induced immunoregulatory cytokine interleukin (IL)-10 in skin as well as in draining lymph nodes, and an elevated amount of IL-12 in draining lymph nodes. These in vivo observations suggest that GTPs are photoprotective, and can be used as pharmacological agents for the prevention of solar UVB light-induced skin disorders associated with immune suppression and DNA damage. (C) 2001 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:109 / 114
页数:6
相关论文
共 64 条
[1]   IDENTIFICATION OF THE MOLECULAR TARGET FOR THE SUPPRESSION OF CONTACT HYPERSENSITIVITY BY ULTRAVIOLET-RADIATION [J].
APPLEGATE, LA ;
LEY, RD ;
ALCALAY, J ;
KRIPKE, ML .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 170 (04) :1117-1131
[2]  
BRASH DE, 1988, PHOTOCHEM PHOTOBIOL, V48, P59
[3]   Ultraviolet B radiation-induced DNA lesions in mouse epidermis: An assessment using a novel P-32-postlabelling technique [J].
Chatterjee, ML ;
Agarwal, R ;
Mukhtar, H .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1996, 229 (02) :590-595
[4]  
DONAWHO CK, 1991, CANCER RES, V51, P4176
[5]  
ELMETS CA, 1992, PHARM SKIN, P389
[6]  
ENK AH, 1993, J IMMUNOL, V151, P2390
[7]  
FIORENTINO DF, 1991, J IMMUNOL, V147, P3815
[8]  
FIORENTINO DF, 1991, J IMMUNOL, V146, P3444
[9]   Activated complement component 3 (C3) is required for ultraviolet induction of immunosuppression and antigenic tolerance [J].
Hammerberg, C ;
Katiyar, SK ;
Carroll, MC ;
Cooper, KD .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (07) :1133-1138
[10]  
Hammerberg C, 1996, J IMMUNOL, V157, P5254