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.

Objective: To investigate the effect and mechanism of ursodeoxycholic acid (UDCA) on the injury of H9c2 cardiomyocytes induced by doxorubicin (DOX). Methods: H9c2 cells were cultured in vitro, H9c2 was treated with 1μM DOX and different concentrations of UDCA, cell viability was determined by CCK-8 method; real-time quantitative polymerase chain reaction was used to detect the expression of cardiomyocyte apoptosis molecule Bax and inflammatory factors IL-1β and IL-6; Western blotting was used to detect the changes in the expression levels of UDCA on DOX-induced cardiomyocyte apoptosis-related proteins Bax, Bcl2, and Caspase3. Results: Compared with the control group, the cardiomyocyte viability of the DOX group was weakened; the expression of inflammatory factors IL-1β and IL-6 were up-regulated; the expression of pro-apoptotic molecules Bax and cleaved Caspase3 were increased; the apoptosis-inhibiting protein Bcl2 was down-regulated (P<0.05). Compared with the DOX group, the UDCA+DOX group significantly restored the vitality of cardiomyocytes; the expression of inflammatory factors IL-1β and IL-6 was down-regulated; the pro-apoptotic molecules Bax and cleaved Caspase3 were down-regulated; the expression of inhibiting apoptosis protein Bcl2 was up-regulated (P<0.05) . Conclusion: UDCA can alleviate the damage of H9c2 cardiomyocytes induced by DOX, and its mechanism may be related to the inhibition of inflammation and apoptosis. This study provides a new experimental basis and theoretical basis for the prevention and treatment of doxorubicin myocardial toxicity. [ABSTRACT FROM AUTHOR]