Cardioprotective Effects of Ginkgetin on Rats with Myocardial Ischemia Reperfusion Injury
QIAN Xiufang1, SUN Huixian1, WANG Chen2, CHEN Ying3
1. Department of Pharmacy, Hospital of Beijing Armed Police Forces, Beijing 100027, China; 2. School of statistics and Mathematics, Shandong University of Finance and Economics, Jinan 250014,China; 3. Fuzhou Jin’an District Traditional Chinese Medicine Hospital,Fuzhou 350013,China
Abstract:Objective To investigate the protective effects of ginkgetin (GK) on myocardial ischemia reperfusion injury (MIRI) in rats and its effects on cardiomyocyte apoptosis.Methods SD rats were divided randomly into sham, model, GK high dose (200 mg/kg) and GK low dose (100 mg/kg) groups. GK was administered by intraperitoneal injection for 7 days before the model operation. Rat model of MIRI was established by coronary artery ligation for 45 min followed by 360 min reperfusion. After the reperfusion, myocardial infarct area (IA), area at risk (AAR) and left ventricle area (LVA) were measured by the NBT staining. The cardiomyocyte apoptosis rate was detected by flow cytometry. The caspase activities in cardiomyocytes were determined by fluorescence method and cardiomyocyte apoptosis factors (Fas and Fas-L) mRNA expression were examined by RT-qPCR.Results GK (200 and 100 mg/kg) significantly reduced IA/AAR and IA/LVA, compared to those of model group (P<0.05 or P<0.01). The cardiomyocyte apoptosis rates in GK groups were evidently reduced (P<0.01). The intracytoplasmic caspase-3 and caspase-8 activities in GK groups were significantly inhibited (P<0.05 or P<0.01). The Fas and Fas-L mRNA expression in GK groups were evidently reduced, which showed significant differences compared to those of model group (P<0.05).Conclusion GK pretreatment shows protective effect on MIRI, which related to preventing the activation of death receptor signaling pathway and inhibition of cardiomyocyte apoptosis.
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