Effects of amiodarone on cardiomyocyte apoptosis and expressions of Bcl2 and Bax protein after ischemia/reperfusion injury in rabbits

AIM:To investigate the effect of amiodarone on cardiomyocyte apoptosis and expressions of Bcl2 and Bax protein after ischemia/reperfusion (I/R) injury in rabbits. METHODS: Sixty mature rabbits were randomized into sham group, I/R group and amiodarone (AM) group with 20 rabbits in each group. I/R group and AM group were subjected to 90 min of occlusion in the left circumflex artery followed by 2 h of reperfusion to establish the myocardial I/R injury model. After 120 min reperfusion, the noreflow (NR) areas were determined by thioflavin S. Apoptosis rate was determined with flow cytometer after AnnexinVfluorescein isothiocyanate (FITC) and propidium iodide (PI) staining. Protein expressions of Bcl2 and Bax were studied by immunohistochemical staining and the ratios of Bcl2/Bax were calculated. RESULTS: The NR area in the AM group decreased significantly compared with the I/R group (t=4483, P<005). The apoptosis rates of cardiomyocyte in both I/R and AM groups were significantly higher than in the sham group (F=80090, P<001). Compared with that in the I/R group, the apoptosis rate of cardiomyocytes significantly decreased in the AM group (F=80090, P<001) and compared with that in sham group, expressions of Bcl2 and Bax protein increased in both I/R and AM groups (F=2901, P<001), (F=21445, P<001). Expression of Bcl2 protein in the AM group was higher (F=2901, P<001) and the expression of Bax protein was significantly lower (F=21445, P<001) than in the I/R group. Compared with that in the I/R group, ratios of Bcl2/Bax increased significantly (F=9761, P<001). CONCLUSION: Amiodarone may improve NR accompanied by inhibiting cardiomyocyte apoptosis induced by I/R injury in rabbits. The mechanism between antiapoptosis and reduction of the NR remains to be further clarified.