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作 者:王飞[1] 赵玉勤[1] 丁国芳[2] 罗李王 张亚茹[1] 杨最素[1]
机构地区:[1]浙江海洋学院食品与医药学院,浙江省海洋生物医用制品工程技术研究中心,浙江舟山316022 [2]浙江省海洋水产研究所,浙江舟山316022
出 处:《浙江海洋学院学报(自然科学版)》2015年第6期582-587,共6页Journal of Zhejiang Ocean University(Natural Science Edition)
基 金:浙江省教育厅项目(Y201225031);浙江海洋学院校级重大项目(X12ZD09);浙江海洋学院科研启动经费资助项目(岩藻黄素对阿霉素药物心脏毒性的保护作用及机理研究)
摘 要:主要探究了岩藻黄素(Fucoxanthin,FUC)对阿霉素(adriamycin,ADR)引起心肌细胞毒性的保护作用。采用DPPH法测定FUC对自由基的清除作用;通过MTT法检测FUC对ADR引起H9C2细胞毒性的保护效果;AO/EB染色法观察H9C2细胞的形态学变化;经Carboxy-DCFDA法测定H9C2细胞内活性氧生成水平变化及Western Blotting检测H9C2细胞凋亡相关蛋白表达。结果表明:DPPH法结果显示FUC具有较强的清除氧自由基能力,IC50小于Vc;FUC对ADR引起的H9C2细胞毒性有较好的保护作用;FUC可以减少ADR引起的H9C2细胞凋亡小体的增加;FUC能抑制由ADR引起的H9C2细胞内活性氧水平升高;FUC可以抑制ADR引起的H9C2细胞内凋亡蛋白Caspase-8水平的下调以及Cleaved Caspase-3、Cleaved PARP水平的上调。结论:FUC具有保护ADR引起心肌细胞毒性的作用,其机理有可能是通过其抗氧化活性抑制ADR引起的心肌细胞氧化应激,进而抑制由ADR引起心肌细胞Caspase-8的活化,进一步抑制由ADR引起的Caspase-3激活及对PARP的剪切来保护心肌细胞的。This paper mainly explored the protective effect of fucoxanthin(FUC) on adriamycin-induced cytotoxicity in cardiac muscle cells. The DPPH method used to determinate the free radical scavenging effect of FUC and MTT assay for detecting the protective effect of FUC on adriamycin-induced cytotoxicity in H9C2 cells. AO/EB staining to observe the morphological changes of H9C2 cells, H9C2 cells in active oxygen generation level changes determined by the Carboxy-DCFDA method and Western blotting detected the expression of apoptosis protein in H9C2 cells. It showed that FUC has strong scavenging oxygen free radical ability in DPPH experiment, with IC50 less than VC; FUC against ADR induced H9C2 cells toxicity effect has a good protection effect; FUC can reduce H9C2 cells apoptotic body increased which induced by ADR; FUC can inhibit the elevated levels of reactive oxygen species in the cells induced by ADR; FUC can inhibit the regulation of ADR induced cardiomyocyte apoptosis protein Caspase-8 up and Cleaved Caspase-3,Cleaved PARP down in H9C2 cells. FUC has the protective effect to cardiac cells toxi-city induced by ADR, and its protective effect is possibly achieved by inhibiting ADR induced oxidative stress in cardiomyocytes by its antioxidant activity, And then inhibited the activation of Caspase-8 induced by ADR, and further inhibited the activation of Caspase-3 induced by ADR and the shear of PARP to protect cardiomyocytes.
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