中文摘要：

目的 观察表没食子儿荼素没食子酸酯（epigallocatechingallate，EGCG）对正常生理代谢状态下人皮肤成纤维细胞（human skin fibroblast，HSF）自然老化以及经长、中波紫外线（UVA及UVB）多次辐射后HSF光损伤的影响。方法 分离新生儿包皮获得原代HSF，将其分为正常生理代谢传代实验组（A组）和多次UV照射实验组（B组）。预实验选定EGCG有效作用质量浓度25mg·L^-1。A组细胞包括加入EGCG干预组和空白对照组，共孵育80d。B组HSF细胞分组包括：空白对照组、EGCG干预组、多次UVA组、多次UVA4-EGCG组、多次UVB组及多次UVB4-EGCG组，其中UVA和UVB均采用文献提示日常生理剂量，每天照射，持续照射2周。采用组织化学染色法检测细胞中衰老相关β-半乳糖苷酶的表达量，观察细胞自然老化及照光后的老化情况；采用流式细胞仪测定细胞周期及细胞凋亡率。结果 A组中，EGCG组的β-半乳糖苷酶阳性细胞数较正常对照组下降了47．60％（P〈0．05）。B组中正常细胞组及EGCG组均只见少量的β-半乳糖苷酶阳性细胞。其余几组阳性细胞比率为：多次UVB组〈多次UVA组〈EGCG4-多次UVB组〈EGCG4-多次UVA组，4组细胞间阳性比率差异均有统计学意义（P〈0．05）。日常剂量UV多次辐射后可上调HSF的凋亡率，经EGCG处理的两组细胞凋亡率与单纯UVB组和单纯UVA组比较分别增加了87．08％和56．92％。结论 EGCG可减缓生理代谢状态下的HSF老化；EGCG可进一步增加UV多次辐射后的细胞老化及细胞凋亡，此可能是EGCG减轻自然老化去除多次光损伤不同机制所致。

英文摘要：

OBJECTIVE To observe the effect of epigallocatethi-3-gallate （EGCG） on cell senescence and chronic photodamage induced by UVA and UVB irradiation in human skin fibroblasts. METHODS Fibroblasts were separated from infant foreskin and divided into long-term culture group（ Group A） and long-term UV irradiation group（ group B ）. Natural cell senescence was conducted in Group A. UV related photodamage was performed in group B, which included group control, EGCG, UVA, UVB, UVA ＋ EGCG and UVB ＋ EGCG. The cells were irradiated by 30 mJ. cm^ -2 UVB and 10 J . cm^ -2 UVA every day for consecutive 2 weeks. The senescence associated β-Gal was detected by histochemical stain. The apoptosis and cell cycle were detected by flow cytometry assay. RESULTS After cells were cultured with EGCG or DMEM for 80 d,the rate of senescence cells in EGCG group was lower than the control group. Long-term UV irradiation increased the rate of senescence cells, but when cells were cultured with EGCG before UV irradiation, the percentage of senescence cells were increased more. Long-term UV irradiation increased the apoptosis rate of human skin fibro- blasts and EGCG increased the UV induced apoptosis rate. CONCLUSION EGCG can decrease the natural cell senescence percentage. EGCG can increase the HSF senescence and apoptosis rate induced by long term UVA and UVB irradiation in HSF.