Protective effects of tea polyphenols and caffeine

被引:49
作者
Camouse, Melissa M.
Hanneman, Kaija K.
Conrad, Edward P.
Baron, Elmo D.
机构
[1] Univ Hosp, Dept Dermatol, Cleveland, OH 44106 USA
[2] Case Western Reserve Univ, Cleveland, OH 44106 USA
关键词
D O I
10.1586/14737140.5.6.1061
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Compounds derived from botanical sources, such as polyphenols from tea, have been of interest as possible therapeutic agents. Their benefits in terms of cancer chemoprevention have also been investigated primarily through in vitro and animal in vivo studies. Ultraviolet light from solar radiation has been proven to initiate and promote skin cancer, which is the most common malignancy in light-skinned populations. This review discusses the effects of tea polyphenols in preventing cutaneous carcinogenesis. Although many of the mechanisms and pathways discussed may be applicable to other carcinogens, this review focuses mainly on those related to ultraviolet light-induced processes and potential action sites for tea polyphenols. Since caffeine is a component of tea, and has also been suggested as a possible chemoprotective agent, it is included in this review. Based on data from numerous studies published in the scientific literature, tea polyphenols are promising chemopreventive agents against ultraviolet-induced skin cancers. Their antioxidant properties, inhibitory effects on signal transduction pathways, cell proliferation, angiogenesis and capacity for apoptosis induction, as well as possible immune protective effects, are among the mechanisms that contribute to skin cancer prevention.
引用
收藏
页码:1061 / 1068
页数:8
相关论文
共 61 条
[1]   Suppression of UVB-induced phosphorylation of mitogen-activated protein kinases and nuclear factor kappa B by green tea polyphenol in SKH-1 hairless mice [J].
Afaq, F ;
Ahmad, N ;
Mukhtar, H .
ONCOGENE, 2003, 22 (58) :9254-9264
[2]   Inhibition of ultraviolet B-mediated activation of nuclear factor κB in normal human epidermal keratinocytes by green tea Constituent (-)-epigallocatechin-3-gallate [J].
Afaq, F ;
Adhami, VM ;
Ahmad, N ;
Mukhtar, H .
ONCOGENE, 2003, 22 (07) :1035-1044
[3]   Cell cycle dysregulation by green tea polyphenol epigallocatechin-3-gallate [J].
Ahmad, N ;
Cheng, PY ;
Mukhtar, H .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2000, 275 (02) :328-334
[4]   THE ROLE OF JUN, FOS AND THE AP-1 COMPLEX IN CELL-PROLIFERATION AND TRANSFORMATION [J].
ANGEL, P ;
KARIN, M .
BIOCHIMICA ET BIOPHYSICA ACTA, 1991, 1072 (2-3) :129-157
[5]   The NF-kappa B and I kappa B proteins: New discoveries and insights [J].
Baldwin, AS .
ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 :649-683
[6]   (-)-epigallocatechin-3-gallate inhibition of ultraviolet B induced AP-1 activity [J].
Barthelman, M ;
Bair, WB ;
Stickland, KK ;
Chen, WX ;
Timmermann, N ;
Valcic, S ;
Dong, ZG ;
Bowden, GT .
CARCINOGENESIS, 1998, 19 (12) :2201-2204
[7]  
Barthelman M, 1998, CANCER RES, V58, P711
[8]  
Bode A M, 2000, Lancet Oncol, V1, P181, DOI 10.1016/S1470-2045(00)00029-2
[9]  
Bromberg J, 2001, METHOD ENZYMOL, V333, P138
[10]   ACTIVATION OF MAP KINASE KINASE IS NECESSARY AND SUFFICIENT FOR PC12 DIFFERENTIATION AND FOR TRANSFORMATION OF NIH 3T3 CELLS [J].
COWLEY, S ;
PATERSON, H ;
KEMP, P ;
MARSHALL, CJ .
CELL, 1994, 77 (06) :841-852