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Aim:To investigate the mechanism of polypeptide from Chlamysfarreri (PCF)protecting HaCaT cells from apoptosis induced by UVA plus UVB in vitro.Methods:An apoptotic model of UV irradiation-induced HaCaT cells wasestablished.The 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromideassay,agarose gel electrophoresis,biochemical methods,and Western blottingwere employed in the study.Results:PCF inhibited the UV irradiation-inducedapoptosis of HaCaT cells.PCF strongly reduced the intracellular reactive oxygenspecies level,enhanced activities of superoxide dismutase and glutathione per-oxidase and increased the total anti-oxidative capacity in HaCaT cells followingUV irradiation.Furthermore,we found that PCF could inhibit the phosphorylationof c-Jun amino-terminal kinase and the activity of caspase-3 in a concentration-dependent manner.Conclusion:PCF protected HaCaT cells from apoptosis in-duced by UVA plus UVB,mainly through decreasing the intracellular ROS leveland increasing the activities of anti-oxidative enzymes to block the ROS-JNK-caspase-3-apoptosis signaling pathway.
Aim: To investigate the mechanism of polypeptide from Chlamys farreri (PCF) protecting HaCaT cells from apoptosis induced by UVA plus UVB in vitro. Methods: An apoptotic model of UV irradiation-induced HaCaT cells wasestablished. The 3- (4,5-dimethyl- 2-thiazolyl) -2,5-diphenyl-2H-tetrazolium bromideassay, agarose gel electrophoresis, biochemical methods, and Western blottingwere employed in the study. Results: PCF inhibited the UV irradiation-inducedapoptosis of HaCaT cells. oxygenspecies level, enhanced activities of superoxide dismutase and glutathione per-oxidase and increased the total anti-oxidative capacity in HaCaT cells following UV irradiation. Fürthermore, we found that PCF could inhibit the phosphorylation of c-Jun amino-terminal kinase and the activity of caspase- 3 in a concentration-dependent manner. Conclusion: PCF protected HaCaT cells from apoptosis in-duced by UVA plus UVB, mainly through reducing the intracellular ROS leveland increase th e activities of anti-oxidative enzymes to block the ROS-JNK-caspase-3-apoptosis signaling pathway.