Molecular mechanism of polypeptides from Chlamys farreri (PCF)鈥檚 anti-apoptotic effect in UVA-exposed HaCaT cells involves HSF1/HSP70, JNK, XO, iNOS and NO/ROS

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• 作者：Xiaowen Wang ; Qixiao Jiang ; Wencheng Wang ; Li Su ; Yantao Han ; Chunbo Wang
• 关键词：Ultraviolet A-induced apoptosis ; Heat shock transcription factor 1 ; Heat shock protein 70 ; c-Jun N-terminal kinases ; Inducible nitric oxide synthase ; Xanthine oxidase
• 刊名：Journal of Photochemistry and Photobiology B: Biology
• 出版年：5 January, 2014
• 年：2014
• 卷：130
• 期：Complete
• 页码：47-56
• 全文大小：2271 K

文摘

This study investigated the molecular mechanisms of polypeptides from Chlamys farreri (PCF)鈥檚 anti-apoptotic effects in ultraviolet A-rays (UVA) exposed HaCaT cells. UVA-induced apoptosis in HaCaT cells was confirmed with Hoechst 33258 fluorescent staining; PCF treatment inhibited UVA-induced apoptosis in HaCaT cells, increased transcriptional activities of heat shock factor protein 1 (HSF1) and the expression of heat shock protein 70 (HSP70), whereas inhibited activation of c-Jun N-terminal kinases (JNK), expression of xanthine oxidese (XO), inducible nitric oxide synthase (iNOS) and release of nitric oxide (NO)/reactive oxygen species (ROS). Meanwhile, the HSF1 transcription inhibitor quercetin increased UVA-induced apoptosis, activation of JNK, expression of XO and iNOS and release of NO/ROS. Among the two NO release peaks we found in UVA exposed HaCaT cells, XO inhibitor oxypurinol was found to be able to inhibit NO release at 3 h post UVA exposure but not 18 h, while iNOS inhibitor S-methylisothiourea sulfate (SMT) was found to inhibit iNOS expression and NO release at 18 h but not 3 h. PCF鈥檚 protection against UVA-induced apoptosis in HaCaT cells involves increased transcriptional activity of HSF1, increased expression of HSP70, and the subsequential inhibition of JNK pathway, XO and iNOS expression and ROS/NO release.