动物实验,心力衰竭,促血小板生成素 z-bo 2020-09-14 388

　　Objective 　 To investigate the effect of thrombopoietin (TPO) on adriamycin-induced heart failure (CHF) rat cardiomyocyte apoptosis and its regulatory mechanism on TGF-β1/Smad3 signaling.

　　"Method" The rats were randomly divided into a control group, a model group, a treatment group, and an inhibitor group. The model group, the treatment group, and the inhibitor group were intraperitoneally injected with adriamycin to construct a heart failure model. The treatment group was intraperitoneally injected with 5μg/kg TPO daily, and the inhibitor group was injected intraperitoneally with 1.2mg/kg SB431542 daily, TUNEL staining, immunofluorescence, Westernblot detection of rat cardiomyocyte apoptosis, Caspase-3, TGF-β1 and p- The expression level of Smad3.

　　Results Compared with the control group, the apoptosis rate of cardiomyocytes in the model group, the expression of TGF-β1, p-Smad3, and Caspase-3 were significantly increased. Compared with the model group, the apoptosis rate of cardiomyocytes in the treatment group and the inhibitor group was The expressions of TGF-β1, p-Smad3, and Caspase-3 were significantly reduced, and the differences were statistically significant (P<0.05).

　　Conclusion 　 TPO can reduce the apoptosis rate of cardiomyocytes in CHF rats caused by doxorubicin. The mechanism may be related to the inhibition of TGF-β1/Smad3 signal.