中文摘要：

背景：扇贝多肽可以通过Fas通路及NF-κB通路发挥对中波紫外线照射后的人角质形成细胞株（HaCaT）的保护作用。目的：观察中波紫外线辐射后HaCaT细胞的凋亡情况和细胞内肿瘤坏死因子α/肿瘤坏死因子受体1的活化情况,以及扇贝多肽的干预作用。方法：实验以20mJ/cm^2中波紫外线辐照HaCaT细胞0.5h建立细胞辐射损伤模型,药物低、中、高剂量组、阳性对照组、抑制剂组分别在造模前2h加入1.42,2.84,5.69mmol/L的扇贝多肽、5.68mmol/L的维生素C及50mg/L的抗肿瘤坏死因子α单克隆抗体。结果与结论：中波紫外线辐照后,HaCaT细胞凋亡增多,肿瘤坏死因子α、肿瘤坏死因子受体1 mRNA及磷酸化JNK蛋白表达量增加;1.42,2.84,5.69mmol/L的扇贝多肽均可降低中波紫外线辐照引起的细胞内肿瘤坏死因子α、肿瘤坏死因子受体1 mRNA及磷酸化JNK表达,抑制HaCaT细胞凋亡,以5.69mmol/L扇贝多肽的作用效果最明显,与5.68mmol/L维生素C的作用相当,且50mg/L抗肿瘤坏死因子α单克隆抗体也可明显降低中波紫外线辐照引起的细胞内磷酸化JNK表达。说明扇贝多肽能抑制中波紫外线辐照引起的HaCaT细胞凋亡,其可以通过肿瘤坏死因子α/肿瘤坏死因子受体1通路发挥抗凋亡作用。

英文摘要：

BACKGROUND：Polypeptide from Chlamys farreri（PCF） exerts protective effects on ultraviolet B radiation-induced human keratinocyte cell line HaCaT cells through Fas pathway and nuclear factor-κB pathway.OBJECTIVE：To investigate HaCaT cell apoptosis after ultraviolet B radiation,and activation of tumor necrosis factor-α/tumor necrosis factor receptor-1,and intervention of PCF.METHODS：Cell injury models were established by 20 mJ/cm2 ultraviolet B radiation on HaCaT cells for 0.5 hour.Low-dose,moderate-dose and high-dose drug groups,positive control group and inhibitor group were treated with 1.42,2.84,5.69 mmol/L PCF,5.68 mmol/L vitamin C and 50 mg/L anti-tumor necrosis factor-α monoclonal antibody.RESULTS AND CONCLUSION：After ultraviolet B radiation,HaCaT cell apoptosis became more.Tumor necrosis factor-α,tumor necrosis factor receptor 1 mRNA and phosphorylated c-Jun N-terminal kinase expression increased.1.42,2.84 and 5.69 mmol/L PCF could reduce ultraviolet B radiation-induced tumor necrosis factor-α,tumor necrosis factor receptor 1 mRNA and phosphorylated c-Jun N-terminal kinase expression,and inhibit cell apoptosis,especially 5.69 mmol/L PCF,which was identical to the effects of 5.68 mmol/L vitamin C.50 mg/L anti-tumor necrosis factor-α monoclonal antibody significantly decreased ultraviolet B radiation-induced phosphorylated c-Jun N-terminal kinase expression.These suggest that PCF inhibited ultraviolet B radiation-induced HaCaT cell apoptosis by tumor necrosis factor-α/tumor necrosis factor receptor 1 pathway.