Title: Effects of amiodarone on cardiomyocyte apoptosis and expressions of Bcl-2 and Bax protein after ischemia/reperfusion injury in rabbits
Abstract: 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.
Publication Year: 2013
Publication Date: 2013-01-01
Language: en
Type: article
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