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首页> 外文期刊>Molecular Biology Reports >Ethyl pyruvate reduces myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein in rats
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Ethyl pyruvate reduces myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein in rats

机译:丙酮酸乙酯通过抑制大鼠高迁移率族box 1蛋白减少心肌缺血和再灌注损伤

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摘要

High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia and reperfusion (I/R) injury. Ethyl pyruvate (EP), a potent reactive oxygen species scavenger, has been reported to inhibit myocardial apoptosis and reduce myocardial I/R injury. The aim of this study was to investigate the mechanism by which EP reduces myocardial I/R injury in rats. Anesthetized male rats were once treated with EP (50 mg/kg, i.p.) before ischemia, and then subjected to ischemia for 30 min followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting. The results showed that pretreatment of EP (50 mg/kg) could significantly reduce the infarct size and the levels of LDH and CK after 4 h reperfusion (all P < 0.05). EP could also significantly inhibit the increase of the MDA level, the decrease of the SOD level (both P < 0.05). Meanwhile, EP could significantly inhibit the expression of HMGB1 induced by I/R. The present study suggested that ethyl pyruvate could attenuate myocardial I/R injury by inhibiting HMGB1 expression.
机译:高迁移率族1盒蛋白(HMGB1)在心肌缺血和再灌注(I / R)损伤中起重要作用。丙酮酸乙酯(EP),一种有效的活性氧清除剂,据报道可抑制心肌细胞凋亡并减少心肌I / R损伤。这项研究的目的是研究EP减少大鼠心肌I / R损伤的机制。麻醉后的雄性大鼠在缺血前先用EP(50 mg / kg,腹腔注射)处理,然后进行30分钟的缺血再灌注4 h。测量了乳酸脱氢酶(LDH),肌酸激酶(CK),丙二醛(MDA),超氧化物歧化酶(SOD)活性和梗塞面积。通过免疫印迹评估HMGB1表达。结果表明,EP预处理(50 mg / kg)可显着减少再灌注4 h后的梗塞面积以及LDH和CK的水平(所有P <0.05)。 EP还可以显着抑制MDA水平的升高和SOD水平的降低(均P <0.05)。同时,EP可以显着抑制I / R诱导的HMGB1的表达。本研究表明丙酮酸乙酯可通过抑制HMGB1表达来减轻心肌I / R损伤。

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