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目的:探讨解偶联蛋白2(uncoupling protein 2,UCP2)在酒精性心肌损害中的作用及其分子机制。方法:采用乙醇在体内的代谢产物乙醛作为刺激因素,将培养心肌细胞分为对照组,乙醛组和乙醛+UCP2抑制剂京尼平组(京尼平组),干预24小时后检测心肌细胞中超氧阴离子(superoxide anion,SOA)及一氧化氮(nitric oxide,NO)的水平,并检测UCP2的蛋白表达水平,另一组实验干预72小时后采用TUNEL法检测心肌细胞凋亡率。结果:与对照组比较,乙醛组心肌细胞中SOA水平显著升高(P<0.01),而NO水平显著降低(P<0.01),且UCP2的蛋白水平也较对照组显著增加(P<0.01)。而与乙醛组比较,京尼平组心肌细胞中SOA的水平进一步增加(P<0.01),NO的水平也进一步降低(P<0.01)。与对照组比较,乙醛可诱导培养心肌细胞凋亡(P<0.01),而京尼平组凋亡率较乙醛组则进一步升高(P<0.01)。结论:UCP2在酒精性心肌损害中通过调控SOA/NO的水平发挥代偿性保护作用。
Objective: To investigate the role of uncoupling protein 2 (UCP2) in alcoholic myocardial injury and its molecular mechanism. Methods: Cardiomyocytes were divided into control group, acetaldehyde group and genipin + genipin group (genipin group) by acetaldehyde, a metabolite of ethanol in vivo. After 24h intervention, The levels of superoxide anion (SO2) and nitric oxide (NO) in myocardial cells were detected and the protein expression of UCP2 was detected. Another group of experimental intervention 72 hours after myocardial cell apoptosis was detected by TUNEL method. Results: Compared with the control group, the level of SOA in cardiomyocytes of acetaldehyde group was significantly increased (P <0.01), NO level was significantly decreased (P <0.01), and the protein level of UCP2 was significantly increased ). Compared with the acetaldehyde group, the level of SOA in the genipin group increased further (P <0.01) and the NO level decreased (P <0.01). Compared with the control group, acetaldehyde induced cardiomyocyte apoptosis (P <0.01), while the apoptosis rate of genipin group was higher than that of acetaldehyde group (P <0.01). CONCLUSIONS: UCP2 exerts a compensatory protective effect by regulating the level of SOA / NO in alcoholic myocardial damage.