中文摘要：

建立了紫外线A和B辐射诱导的永生化角质形成细胞（HaCaT）凋亡的模型，采用四甲基偶氮唑盐法、琼脂糖凝胶电泳、流氏细胞仪、酶化学方法和蛋白印迹等技术，研究了扇贝多肽（Pcr）抑制紫外线诱导HaCaT细胞凋亡的分子机制。实验发现，PCF可明显抑制紫外线A和B诱导的HaCaT细胞凋亡。1．42～5．68mM剂量范围内PCF剂量依赖性抑制紫外线诱导的HaCaT细胞内活性氧的生成，并能提高细胞内抗氧化酶活性，增强细胞总抗氧化能力，减少脂质过氧化产物的产生；同时，PCF也抑制细胞内JNK蛋白的磷酸化及Caspases．3蛋白的活化。通过加入ROS、JNK和Caspase．3抑制剂证实，PCF作为抗氧化剂减少了细胞内ROS的生成并提高了细胞内抗氧化酶活性，进而阻断了ROS—JNK—cas—pase-3信号级联反应，抑制了紫外线辐射诱导的HaCaT细胞凋亡。

英文摘要：

We established an apoptotic model of HaCaT cells induced by UVA and UVB to investigate the inhibition mechanism of polypeptide from Chlamys farreri （PCF） by the way of 3-（4,5-dimethyl-2thiazoyl）-2,5-diphenyl-2H-tetrazolium bro- mide assay, Flow cytometry, and Western blotting. The experimental data suggested that PCF can attenuate the apoptosis stress induced by UVA and UVB in HaCaT cells. PCF treatment also can inhibit the reactive oxygen species （ROS） gen- eration, increase the activity of the anti-oxidative enzymes, lower the lipid peroxidation, decrease the phosphorylation of c-Jun amino-terminal kinase （JNK）, and inhibit the activity of Caspases-3 in a dose-dependant manner. By using in- hibitors for ROS, JNK and Caspase-3, it was found that there was the strong relation between PCF with ROS, JNK and Caspase-3. The data suggested that PCF might ameliorate the oxidative stress induced by UVA plus UVB to attenuate the apoptosis stress by JNK-Caspase pathway.