期刊
JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH
卷 15, 期 3, 页码 244-252出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/10286020.2012.762358
关键词
myocardial ischemiareperfusion; salidroside; signal transduction; apoptosis
资金
- Natural Science Foundation of China [81001561]
To investigate the cardioprotective effects of salidroside on myocardial ischemiareperfusion injury (IRI) in rabbits and the underlying action mechanisms in PI3K/Akt signaling pathway, a rabbit ischemia/reperfusion model was created by ligating the left anterior descending coronary arterial branch for 30min and by releasing the ligature to allow reperfusion for 120min. Salidroside or salidroside+PI3K inhibitor (LY294002) was administered via intracoronary injections at the onset of reperfusion. Apoptosis of cardiomyocytes was assessed by terminal dUTP nick-end labeling assay, and the expression of apoptosis-related proteins was observed by immunohistochemistry. The expressions of total Akt and phosphorylated Akt (p-Akt) were detected by western blot analysis. The results showed that intracoronary injection of salidroside at the onset of reperfusion markedly reduced the apoptosis of cardiomyocytes, significantly increasing Bcl-2 and p-Akt proteins expressions and decreasing Bax and caspase-3 expressions in the hearts subjected to ischemia followed by 120-min reperfusion. However, the anti-apoptotic effect induced by salidroside was inhibited by LY294002, which blocked the activation of Akt. These results suggested that intracoronary administration of salidroside at the onset of reperfusion could significantly reduce the IRI-induced apoptosis of cardiomyocytes, and this protective mechanism seemed to be mediated by the PI3KAkt signaling pathway.
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