中波紫外线诱导HaCaT细胞凋亡与扇贝多肽的影响:肿瘤坏死因子α/肿瘤坏死因子受体1通路的研究

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20 mJ/cm2中波紫外线辐照HaCaT 细胞0.5 h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2 h加入1.42,2.84,5.69 mmol/L 的扇贝多肽、5.68 mmol/L 的维生素C及50 mg/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;1.42,2.84,5.69 mmol/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5.69 mmol/L 扇贝多肽的作用效果最明显,与5.68 mmol/L维生素C的作用相当,且50 mg/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.%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.