Polypeptide from Chlamys farreri inhibits UVB-induced apoptosis of HaCaT cells via iNOS/NO and HSP90

来源 :Chinese Journal of Oceanology and Limnology | 被引量 : 0次 | 上传用户:fengeryqq
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Polypeptide from Chlamys farreri(PCF) is a novel marine bioactive product that was isolated from the gonochoric Chinese scallop Chlamys farreri,and was found to be an effective antioxidant in our recent studies.In this study,we investigated the effect of PCF on ultraviolet B(UVB)-induced apoptosis of HaCaT cells and the intracellular signaling pathways involved.Pretreatment with the inducible nitric oxide synthase(iNOS) inhibitor S-methylisothiourea sulfate inhibited UVB-induced apoptosis,indicating that iNOS and NO play important roles in apoptosis.On the other hand,the inhibition of UVB-induced apoptosis in the immortalized keratinocyte(HaCaT) cells by PCF was estimated using a DNA ladder.PCF treatment inhibited UVB-induced iNOS activation,as determined by RT-PCR,NO production,as determined by ESR,and up-regulated heat shock protein(HSP) 90 activation,as determined by Western blotting.Our results indicate that iNOS and NO are involved in UVB-induced apoptosis of HaCaT cells and the protective effect of PCF against UVB irradiation is exerted by suppressing the expression of iNOS,followed by inhibition of NO release and enhanced activation of HSP90. Polypeptide from Chlamys farreri (PCF) is a novel marine bioactive product that was isolated from the gonochoric Chinese scallop Chlamys farreri, and was found to be an effective antioxidant in our recent studies. In this study, we investigated the effect of PCF on ultraviolet B (UVB) -induced apoptosis of HaCaT cells and the intracellular signaling pathways involved. Treatment with the inducible nitric oxide synthase (iNOS) inhibitor S-methylisothiourea sulfate inhibited UVB-induced apoptosis, indicating that iNOS and NO play important roles in apoptosis. On the other hand, the inhibition of UVB-induced apoptosis in the immortalized keratinocyte (HaCaT) cells by PCF was estimated using a DNA ladder. PCF treated inhibited UVB-induced iNOS activation, as determined by RT-PCR, NO production, determined determined by ESR , and up-regulated heat shock protein (HSP) 90 activation, as determined by Western blotting. Our results indicate that iNOS and NO are involved in UVB-induced apoptosis of HaCaT cells and the p rotective effect of PCF against UVB irradiation is exerted by suppressing the expression of iNOS, followed by inhibition of NO release and enhanced activation of HSP90.
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