Study On The Effects Of Butylphthalide On Cardiac Function In Rats

Objective: To investigate the effect of butylphthalide on rat heart function and its possible mechanism.Methods: Wistar rat suckling rats(2 days old)were used to extract primary cardiomyocytes.Firstly,the model of adriamycin myocardial cell injury was screened,then the toxicity of butylphthalide was detected.Finally,the model of adriamycin myocardial cell injury was constructed with the selected concentration of adriamycin,and the effectiveness of butylphthalide on myocardial cell injury model was tested within the non-toxic range of butylphthalide.Mature wistar rats(6 weeks old)were selected to establish adriamycin-induced heart failure model in vivo.Butylphthalide interfered with normal rats and adriamycin-induced heart failure rats.Then high frequency echocardiography was used to detect cardiac function.Pathological sections of cardiac tissue were taken,HE staining,Masson staining and transmission electron microscopy were used to observe the myocardial status of each group.Western blot was used to detect the expression of related proteins.Result: 1.In vitro experiments: MTT results of adriamycin myocardial damage screening showed that adriamycin had a significant inhibitory effect on the viability of primary myocardial cells of Wistar rats(p < 0.001);MTT results of butylphthalide toxicity showed that butylphthalide above 100 mol/L concentration was toxic to primary myocardial cells of Wistar rats(p< 0.01);MTT results of butylphthalide validity test showed that adriamycin model group was fine.Cell viability was significantly lower than that of blank control group.The cell viability in different concentration(1-75 mol/L)of butylphthalide group was significantly higher than that in adriamycin model group(p< 0.001,p< 0.01,p< 0.05).2.In animal experiments,butylphthalide had no significant effect on ejection fraction(EF)and fractional shortening(FS)in normal rats(p>0.05),significantly increased EF and FS values in adriamycin-induced heart failure rats(p<0.001,p<0.01),improved myocardial injury and myocardial fibrosis in adriamycin-induced heart failure rats,and inhibited adriamycin-induced heart failure rats.The expression of Smad3 in myofibrosis-related protein p<0.001).Conclusion: Butylphthalide had no significant adverse effects on cardiac function in rats;Butylphthalide had an improvement in cardiac function in rats with adriamycin-induced heart failure,and its mechanism may be through inhibition of myocardial fibrosis.