ABSTRACT
Objective To explore the potential mechanism of Fasudil hydrochloride pharmacologic postconditioning that alleviated acute myocardial ischemia/reperfusion injury (MI/RI) in rats,narrowed the scope of infacted myocardium,and inhibited cell apoptosis.Methods Ninety rats were randomly and averagely divided into 5 groups:sham group,ischemia/reperfusion (I/R) group,ischemic postconditioning (IPost) group,fasudil hydrochloride (FH) group,and FH and PI3K inhibitor (LY294002) (FH + I) group.The expressions of Rho associated coiled-coil forming protein kinase-1 (ROCK-1),Bcl-2,Bax,Caspase-3,Akt,and P-Akt in rat myocardial cells were determined.Results Compared to I/R group (ROCK1:2.94 ± 0.13),ROCK1 expression was not changed in IPost group (ROCK1:2.79 ± 0.11),FH group (ROCK1:2.83 ± 0.10),and FH + I group (ROCK1:2.85 ± 0.26).Compared to I/R group (Bcl-2:1.11 ± 0.12,P-Akt:1.09 ± 0.06,Bax:1.74 ± 0.06,and caspase-3:1.32 ± 0.12),the expressions of Bcl-2 and P-Akt in FH group (Bcl-2:1.76 ± 0.08,and P-Akt:1.73 ± 0.05) and IPost group (Bcl-2:1.74 ± 0.06,and P-Akt:1.37 ± 0.05) were all significantly higher than those in I/R group (P ＜ 0.05),while the expressions of Bax and caspase-3 in FH group (Bax:0.98 ±0.14,and caspase-3:0.97 ±0.06) and IPost group (Bax:0.97 ±0.11,and caspase-3:1.07 ±0.08) were all significantly lower than those in I/R group (P ＜0.05).Compared to FH group,the expressions of Bcl-2 and P-Akt in FH + I group (Bcl2:1.05 ±0.12,and P-Akt:1.21 ±0.06) were decreased (P ＜0.05),while the levels of Bax and caspase-3 (Bax:1.61 ±0.11,and caspase-3:1.42 ± 0.11) were increased (P ＜ 0.05).Conclusions The mechanism of FH postconditioning was associated with the inhibition of ROCK activity,and the activation of PI3K-Akt pathway.