Inhibition of UVA-induced apoptotic signaling pathway by polypeptide from Chlamys farreri in human HaCaT keratinocytes

文献类型： 外文期刊

第一作者： Li, Jin-Lian

作者： Li, Jin-Lian;Liu, Ning;Chen, Xue-Hong;Sun, Mi;Wang, Chun-Bo

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期刊名称：RADIATION AND ENVIRONMENTAL BIOPHYSICS （ 影响因子：1.925； 五年影响因子：1.926 ）

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收录情况： SCI

摘要： Chronic UVA irradiation has been reported to induce photoaging and photocarcinogenesis.UVA is a potent inducer of reactive oxygen species(ROS),which can induce various biological processes,including apoptosis.Polypeptide from Chlamys farreri(PCF)is a novel marine active material isolated from the gonochoric Chinese scallop C.farreri.In our previous studies,PCF was found to be an effective antioxidant inhibiting UVA-induced ROS production and a potential inhibitory agent for UVA-induced apoptosis in the human keratinocyte cell line HaCaT.The intracellular mechanisms of how PCF protects HaCaT cells from UVA-induced apoptosis are not understood.Thus,we here investigate the effect of PCF on UVA-induced intracellular signaling of apoptosis.Pretreatment with the ROS scavenger N-acetylcysteine(NAC),the p38 MAPK inhibitor SB203580 or the caspase-3 inhibitor Ac-DEVD-CHO was found to effectively prevent UVA-induced apoptosis,indicating that ROS,p38 MAPK and caspase-3 play important roles in apoptosis.H2O2-induced apoptosis was attenuated by PCF,suggesting that PCF plays its anti-apoptotic role through its antioxidant activity.In addition,PCF treatment inhibited UVA-induced p38 MAPK activation and caspase-3 activation,as assayed by Western blot analysis and flow cytometry,respectively.Our results suggest that PCF attenuates UVA-induced apoptosis through a reduction of ROS generation and diminished p38 MAPK and caspase-3 activation.

分类号： O644

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