紫外线诱导成纤维细胞凋亡及防护机制的初步探讨

目的 探讨紫外线诱导真皮成纤维细胞凋亡的发生机理以及绿茶多酚的主要成分表没食子儿茶素没食子酸酯(EGCG)对凋亡的保护作用。方法 用流式细胞仪及RT-PCR方法分别检测了成纤维细胞凋亡率变化以及凋亡相关基因Fas和Bcl-2 mRNA表达变化。结果 经中波紫外线(UVB)和长波紫外线(UVA)辐射的成纤维细胞,均在G1期前出现明显的亚二倍体(凋亡峰),凋亡率分别为34.79±2.24和29.69±3.05;而应用EGCG后凋亡率均明显下降为4.23±0.03和5.23±0.01。经统计学分析,差异有显著性(P<0.001)。Fas的mRNA表达在UVB及UVA辐射组均有较明显增加,分别为0.72±0.05和0.68±0.02;应用EGCG后,两组表达均明显减弱为0.35±0.02和0.47±0.03。经统计学分析,差异有显著性(P<0.001)。Bcl-2的mRNA经UVB辐射后,没有明显变化,仍有较强表达;而经UVA辐射以后,其mRNA表达明显减弱。为0.27±0.03,应用EGCG后,表达则又明显增强为0.51±0.04。结论 EGCG对UVB及UVA诱导的凋亡均有保护作用,但凋亡的发生机理以及保护机理则有所差异。

Mechanism of Fibroblast Apoptosis Induced by Ultraviolet and Its Prevention

Objective To explore the mechanism of ultraviolet-induced fibroblast apoptosis and the protective effects of EGCG, a major green tea catechin, on it. Methods The apoptosis rate of fibroblasts was detected by flow cytometer. The mRNA levels of Fas and Bcl-2 were determined by reverse transcrip-tion-polymerase chain reaction (RT-PCR). Results Apoptosis peak was observed in fibroblast group either treated with ultraviolet A(UVA)or ultraviolet B(UVB), respectively. After treating with EGCG, the apoptosis rate was decreased obviously, with statistical significance (P<0.001). The mRNA level of Fas was elevated after UVA or UVB irradiation and was inhibited by EGCG treatment. The mRNA expression of Bcl-2 was decreased after UVA irradiation, but without obvious difference between the UVB group and the control group. Conclusion EGCG treatment can protect the fibroblast from apoptosis induced by UVA or UVB, with some difference in the mechanism.