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Protective effects of fentanyl preconditioning on cardiomyocyte apoptosisinduced by ischemia-reperfusion in rats

机译:芬太尼预处理对心肌细胞凋亡的保护作用。大鼠缺血再灌注诱导

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摘要

We aimed to study the effect of fentanyl (Fen) preconditioning on cardiomyocyte apoptosis induced by ischemia-reperfusion (I/R) in rats. A total of 120 Sprague Dawley male rats (age: 3 months) were randomly divided into: sham operation group (S group), I/R group, normal saline I/R group (NS group), and fentanyl low, middle, and high dose groups (Fen1: 2 μg/kg; Fen2: 4 μg/kg; Fen3: 6 μg/kg). Heart rate (HR), mean arterial pressure (MAP), left ventricular developed pressure (LVDP), ±dp/dtmax, malondialdehyde (MDA), superoxide dismutase (SOD) activity, creatine phosphokinase-MB (CK-MB), and cardiac troponin-I (cTnI) were measured. Myocardial ischemic (MI) area, total apoptotic myocardial cells, and protein and mRNA expressions of B-cell lymphoma 2 (Bcl-2) and Bax were detected. HR and MAP were higher, while LVDP and ±dp/dtmax were close to the base value in the Fen groups compared to those in the I/R group. Decreased MDA concentration and CK-MB value and increased SOD activity were found in the Fen groups compared to the I/R group, while cTnI concentration was significantly lower in the Fen1 and Fen2 groups (all P<0.05). Myocardial damage was less in the Fen groups compared to the I/R group and the MI areas and apoptotic indexes were significantly lower in the Fen1 and Fen2 groups (all P<0.05). Furthermore, significantly increased protein and mRNAexpressions of Bcl-2, and decreased protein and mRNA expressions of Bax were found inthe Fen groups compared to the I/R group (all P<0.05). Fentanyl preconditioningmay suppress cardiomyocyte apoptosis induced by I/R in rats by regulating Bcl-2 andBax.
机译:我们旨在研究芬太尼(Fen)预处理对大鼠缺血再灌注(I / R)诱导的心肌细胞凋亡的影响。将120只Sprague Dawley雄性大鼠(年龄:3个月)随机分为:假手术组(S组),I / R组,生理盐水I / R组(NS组)和芬太尼低,中,高剂量。高剂量组(Fen1:2μg/ kg; Fen2:4μg/ kg; Fen3:6μg/ kg)。心率(HR),平均动脉压(MAP),左心室发育压(LVDP),±dp / dtmax,丙二醛(MDA),超氧化物歧化酶(SOD)活性,肌酸磷酸激酶-MB(CK-MB)和心脏测量肌钙蛋白-I(cTnI)。检测心肌缺血(MI)区,总凋亡心肌细胞以及B细胞淋巴瘤2(Bcl-2)和Bax的蛋白和mRNA表达。与I / R组相比,Fen组的HR和MAP较高,而LVDP和±dp / dtmax接近基本值。与I / R组相比,Fen组的MDA浓度和CK-MB值降低,SOD活性增加,而Fen1和Fen2组的cTnI浓度则显着降低(所有P <0.05)。与I / R组相比,Fen组的心肌损伤更少,而Fen1和Fen2组的MI区域和凋亡指数则显着降低(所有P <0.05)。此外,蛋白质和mRNA显着增加Bcl-2的表达,Bax蛋白和mRNA的表达降低;Fen组与I / R组相比(所有P <0.05)。芬太尼预处理可能通过调节Bcl-2和Bcl-2抑制I / R诱导的大鼠心肌细胞凋亡巴克斯

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