岩藻黄素对阿霉素引起心肌细胞毒性的保护作用探讨

Protective effect of fucoidin on adriamycin-induced cardiomyocyte cytotoxicity

目的就岩藻黄素(FUC)对阿霉素（ADR）引起的心肌细胞毒性所起的保护作用机制进行分析。方法运用DPPH法研究FUC对自由基所起到的清除作用，采用MTT法研究FUC对ADR引起的H9C2细胞毒性所起到的保护作用，H9C2细胞形态学变化采用AO/EB染色法观察，H9C2细胞内活性氧生成水平变化与H9C2细胞凋亡相关蛋白表达使用Carboxy-DCFDA法与WesternBlotting检测。结果经DPPH法检测发现FUC对氧自由基具有较强清除力，对ADR引起的H9C2细胞毒性FUC发挥着良好保护作用，FUC对ADR引起的H9C2细胞毒性所起到的保护作用机制为减少ADR引起的H9C2细胞凋亡小体增加，使ADR引起的H9C2细胞内活性氧水平升高、H9C2细胞内凋亡蛋白Caspase-8水平下调、CleavedCas-pase-3、CleavedPARP水平上调受抑。结论FUC对ADR引起的心肌细胞毒性所起到的保护作用是通过自身所具有的抗氧化活性使ADR引起的心肌细胞氧化应激受抑，阻断ADR引起心肌细胞Caspase-8活化路径，由此实现对ADR引起的Caspase-3激活与对PARP剪切的有效抑制这一连续过程而实现的。

Objective To investigate the protective effect of FUC on adriamycin(ADR)-induced myocardial cell toxicity.Methods UsingDPPH FUC method to study the scavenging effect on free radicals play a protective role of H9C2,MTT method is used to study the cytotoxicity ofFUC on ADR induced by the H9C2cell morphological changes were observed by AO/EB staining,the expression of H9C2in cells of ROS levelsand H9C2cell apoptosis related protein Carboxy-DCFDA Western and Blotting detection method.Results DPPH assay showed that FUC hasstrong scavenging of oxygen free radicals,FUC to play a good protective effect H9C2cytotoxicity caused by ADR and mechanism of apoptosisin H9C2cells were cytotoxic FUC protective effect of H9C2on ADR induced by the reduced ADR induced increase,elevated levels of reactiveoxygen species that caused by ADR the H9C2cells and H9C2cells apoptosis protein Caspase-8Cleaved Cas-pase-3,Cleaved and downreguLationof PARP upreguLation inhibited.Conclusion The protective effect of FUC on myocardial cell toxicity caused by ADR is played by oxidative stressin myocardial cells by antioxidant activity has its own ADR induced inhibition of blocked ADR induced myocardial cell activation of Caspase-8pathway,thereby effectively inhibit ADR induced Cas-pase-3activation and PARP shear this continuous process to achieve.