中文摘要：

目的从凋亡相关分子Fas（CD95）、Fas相关死亡结构域（Fasassociated protein with death domain。FADD）及半胱天冬酶-8（caspase-8）的角度，研究扇贝多肽（polypeptide from Chlamys farreri，PCF）抑制紫外线B（Ultraviolet B。UVB）诱导的人角质形成细胞株（immortalized human keratino，HaCaT）细胞凋亡的作用机制。方法实验设计为6组：对照组、UVB模型组、UVB＋5．68mmol·L^-1维生素C阳性对照组、UVB＋5．69mmol·L“PCF组、UVB＋2、84mmol·L^-1 PCF组、UVB＋1、42mmol·L^-1 PCF组。以正交实验设计确立UVB诱导的HaCaT细胞凋亡模型；琼脂糖凝胶电泳和荧光染色（Hoechst33258）分析PCF对UVB诱导的HaCaT细胞凋亡的影响；琼脂糖凝胶电泳分析caspase-8抑制剂（z-IETD-fmk）对UVB诱导的HaCaT细胞凋亡的影响；逆转录-聚合酶链反应（Reverse Transcription-Polymerase Chain Reaction，RT-PCR）检测Fas（CD95）mRNA的表达；蛋白质印迹法检测FADD及caspase-8蛋白的表达。结果PCF能明显抑制UVB引起的HaCaT细胞凋亡；z-IETD-fmk对UVB诱导的HacaT细胞凋亡有明显抑制作用；1．42-5．69mmol·L^-1内的PCF可剂量依赖性抑制UVB引起的Fas,FADD的表达增加及caspase-8的活化。结论PCF可剂量依赖性抑制UVB诱导的HaCaT细胞凋亡。其作用机制与抑制Fas，FADD的表达及caspase-8的活化有关。

英文摘要：

OBJECTIVE To investigate the inhibition effect of polypeptide from Chlamys farreri （PCF） on from UVB-induced apoptosis of HaCat cells through Fas and Fas-assoeiated protein with death domain （FADD） and easpase-8. METHODS Experiments design were divided into six groups： control group, UVB model group, UVB ＋ 5.68 mmol · L ^-1 vitamine C positive control group, UVB＋5.69 mmol·L^-1 PCF group, UVB ＋2.84 mmol · L^-1 PCF group, UVB ＋ 1.42 mmol · L^-1 PCF group. UVB-indueed apoptotie model of HaCaT cells was established by orthogonal design. Using agarose gel eleetrophoresis and fluorescence staining （Hoeehst 33258）, the effects of PCF on UVB-indueed apoptosis of HaCaT cells were investigated. Using agarose gel eleetrophoresis, the effects of easpase-8 inhibitor z-IETD-fmk on UVB-indueed apoptosis of HaCaT cells were investigated. Expression levels of Fas （C1）95） mRNA were detected by RT-PCR. Expression levels of FADD and easpase-8 were determined by Western blot analysis. RESULTS PCF significantly protected against UVB-indueed apoptosis of HaCaT cells, z-IETD-fmk had inhibitory effects on UVB- induced apoptosis of HaCaT cells. PCF inhibited the expression of Fas and FADD and activation of easpase-8 dose-dependently. CONCLUSION PCF could protect HaCaT cells from UVB-indueed apoptosis dose-dependently. Its inhibitory effect on apoptosis may attributes to inhibition expression of Fas and FADD and activation of caspase-8.