Vol 20, No 2 (2013)
Original articles
Published online: 2013-04-05
Protective effects of fasudil hydrochloride post-conditioning on acute myocardial ischemia/reperfusion injury in rats
DOI: 10.5603/CJ.2013.0034
Cardiol J 2013;20(2):197-202.
Abstract
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.
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.
Keywords: fasudil hydrochloride (FH)ischemia/reperfusionpost-conditioning
