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Objectives: To investigate the effects of fasudil (Fas) on myocardial hypertrophy in rats. Methods Rats were randomly divided into 5 groups: control , transverse aortic constriction (TAC) model, Fas (5mg/kg) plus TAC, TAC plus Fas(20mg/kg), and TAC plus captopril (Cap, positive drug). After administering treatments for eight weeks, myocardial intracellular Ca 2 + ion, cardiac hemodynamic parameters and histological changes, as well as NO and SOD levels of serum were measured. Protein expression changes in Caspase-3 and Bcl-2 were detected. Results Compared with the control group, rats in the TAC group showed increases in cardiac and left ventricular weight indexes, and had larger myocardial fiber diameters, as well as an increased incidence of myocardial fibrosis. Treatment of TAC-induced rats with Fas and Cap reduced the degree of these changes, improving myocardial contraction and relaxation functions, and significantly (p<0.05) reducing the free Ca 2+ ion concentration of myocytes. The results indicated that Fas or Cap treatment can alleviate myocytes apoptosis. Furthermore, increasing expression of Caspase-3 and decreasing expression of Bcl-2 were observed in the TAC model group, and these changes could be alleviated by treatment with Fas and Cap. Conclusions Fas treatment significantly improved cardiac hypertrophy, which might be related to modulating the expression of Caspase-3 and Bcl-2 protein, enhancement of NO release of myocytes in rats after TAC

Fasudil Protects Against the Myocardial Hypertrophy of Transverse Aortic Constriction Via Modulating the Expression of Caspase-3 and Bcl-2 Protein