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Exogenous NADPH ameliorates myocardial ischemia–reperfusion injury in rats through activating AMPK/mTOR pathway

机译:外源性NADPH通过激活AMPK / MTOR途径改善大鼠心肌缺血再灌注损伤

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摘要

NADPH reduced myocardial I/R-induced injury in rats. Myocardial I/R was established by ligating the left anterior descending artery in rats. NADPH 4, 8, and 16 mg/kg (N4, N8, and N16) and diltiazem were administered intravenously at the onset of reperfusion. The infarct size was evaluated 2 h after reperfusion. Representative photographs (a) and quantitative analysis (b) showed that NADPH decreased the infarct size. AAR area at risk, IS infarct size, LV left ventricle. c Cardiac function was evaluated by serum LDH at 2 h and cTn-I at 4 h after reperfusion. LDH lactate dehydrogenase, cTn-I cardiac troponin I. n = 6~8 rats. The bars represent the mean ± SD, *P < 0.05, **P < 0.01, ***P < 0.001 compared with the I/R group
机译:NADPH降低了大鼠心肌I / R诱导的损伤。通过在大鼠中连接左前期下降动脉来建立心肌I / R.在再灌注开始时静脉内施用NADPH 4,8和16mg / kg(N4,N8和N16)和Diltizem。再灌注后,梗塞大小评价2小时。代表性照片(A)和定量分析(B)表明NADPH降低了梗塞尺寸。 AAR面积有风险,是梗塞大小,LV左心室。 C再灌注后4小时,通过2小时和CTN-1评估C心脏功能。 LDH乳酸脱氢酶,CTN-I心肌肌钙蛋白I. n = 6〜8大鼠。与I / R组相比,杆代表平均值±SD,* P <0.05,** P <0.01,*** P <0.001

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