Protective effects of fasudil hydrochloride post-conditioning on acute myocardial ischemia/reperfusion injury in rats.

BACKGROUND

In recent years, the alleviation of acute myocardial ischemia and reperfusion injury (MI/RI) during myocardial reperfusion has presented a significant clinical challenge. This study was performed to investigate the effects of fasudil hydrochloride (FH) postconditioning on MI/RI and the underlying mechanism.

METHODS

Seventy-two rats were randomly divided into four groups: a Sham group, an ischemia/reperfusion (I/R) group, a fasudil hydrochloride (FH) group, and a fasudil hydrochloride+PI3K inhibitor (FH+I) group. Myocardial infarct size, cell apoptotic index (AI), and myocardial tissue expression of Rho-associated coiled-coil containing protein kinase 1 (ROCK1), Bcl-2, Bcl-2 associated X protein (Bax), caspase-3, Akt and phosphorylated Akt (P-Akt) were detected.

RESULTS

All these parameters, except Akt expression, were higher in the I/R group than in the Sham group (p < 0.05). Compared to the I/R group, myocardial infarct size, AI, Bax and caspase-3 expression were significantly reduced in the FH group (p < 0.05), while Bcl-2 expression was increased (p < 0.05). However, the myocardial infarct size and AI of the FH+I group were similar to those of the I/R group (p > 0.05). Compared to the FH group, Bcl-2 expression was reduced in the FH+I group, while Bax and caspase-3 expression was increased (p < 0.05). Furthermore, P-Akt expression in the FH group was significantly higher than that of the I/R group (p < 0.05).

CONCLUSIONS

FH post-conditioning alleviated MI/RI, with narrowing of the infarct size and decreased apoptosis of ischemic cardiocytes. The mechanism was associated with activation of the PI3K-Akt signaling pathway.