熊去氧胆酸对阿霉素诱导的H9c2心肌细胞的影响及机制研究

目的:探讨熊去氧胆酸(UDCA)对阿霉素(DOX)诱导的H9c2心肌细胞损伤的影响及机制.方法:体外培养H9c2细胞,1 μMDOX和不同浓度UDCA处理H9c2,CCK-8法测定细胞活力;实时定量聚合酶链反应检测心肌细胞凋亡分子Bax及炎症因子IL-1β、IL-6的表达;Western blotting检测UDCA对...

Effects of Ursodeoxycholic Acid on Doxorubicin-induced Injury in H9c2 Cardiomyocytes and Its Mechanism

Objective: To investigate the effect of Ursodeoxycholic Acid(UDCA) on doxorubicin(DOX)-induced cardiotoxicity in H9 c2 cardiomyocytes and the mechanisms. Methods: The H9 c2 cardiomyocytes were treated with DOX with or without UDCA of different doses. The cell viability was measured by CCK-8 assay, and the inflammatory factors were examined by quantitative real-time polymerase chain reaction(qRT-PCR). As for apoptosis, Western blotting, qRT-PCR were used to analyze. Results: Compared with control group, the viability of H9 c2 cells, the anti-apoptotic protein Bcl2 were decreased(P<0.05). Additionally, the release of inflammatory factors(IL-1β, IL-6), apoptotic molecules(Bax and Cleaved Caspase3) was increased(P<0.05). Compared with DOX group, UDCA+DOX group restored the cell viability, ameliorated the release of inflammatory factors(IL-1β, IL-6), inhibited pro-apoptotic molecules(Bax and Cleaved Caspase3), promoted anti-apoptotic molecules Bcl2 as well(P<0.05). Conclusions: UDCA suppresses DOX-induced injury in H9 c2 cardiomyocytes by reducing inflammation and apoptosis, which provides a pivotal theoretical basis for the clinical application of UDCA in the prevention and treatment of DOX-induced cardiotoxicity.