Protective effect of glycyrrhizin on myocardial ischemia/reperfusion injury-induced oxidative stress, inducible nitric oxide synthase and inflammatory reactions through high-mobility group box 1 and mitogen-activated protein kinase expression
Protective effect of glycyrrhizin on myocardial ischemia/reperfusion injury-induced oxidative stress, inducible nitric oxide synthase and inflammatory reactions through high-mobility group box 1 and mitogen-activated protein kinase expression
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DOI：
10.3892/etm.2017.4617
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发表时间：
2017-08-01
影响因子：
2.7
通讯作者：
Chen, Shuying
中科院分区：
文献类型：
--
作者：
Cai, Xiangna;Wang, Xin;Chen, Shuying
甘草素是一种多年生豆科植物的根茎，在包括中国在内的亚洲各国都有应用。中国，印度和日本，几千年来。本研究通过高迁移率族蛋白1（HMGB 1）和丝裂原活化蛋白激酶（MAPK）的表达，探讨了白藜芦醇苷通过氧化应激、诱导型一氧化氮合酶（iNOS）和炎症反应对心肌缺血/再灌注（I/R）损伤的保护作用。将Sprague-Dawley大鼠分为5组：假手术组;心肌I/R损伤+未治疗组;心肌I/R损伤+ 2 mg/kg麦考汀组;心肌I/R损伤+ 4 mg/kg麦考汀组;和心肌I/R损伤+ 10 mg/kg麦考汀组。预处理组心肌缺血再灌注损伤大鼠心肌梗死面积明显缩小，肌酸激酶、肌酸激酶同工酶、乳酸脱氢酶和心肌肌钙蛋白T活性明显降低。此外，Escherin治疗显着抑制氧化应激，诱导型一氧化氮合酶蛋白表达和炎症反应，在大鼠心肌I/R损伤。此外，在心肌I/R损伤的大鼠中，用Escherichin治疗显著减少HMGB 1从大脑皮层释放到血清中。在心肌I/R损伤模型中，Escherin显著抑制p-ERK、p-p38 MAPK和p-c-Jun N-末端激酶蛋白的表达，促进细胞外信号调节激酶蛋白的表达。总的来说，本研究表明，Escherin的保护作用可能通过氧化应激，iNOS和炎症反应，通过HMGB 1和MAPK表达减少心肌I/R损伤。
Glycyrrhizin, which is a type of perennial leguminous caudex, has been used in various Asian countries, including P. R. China, India and Japan, for thousands of years. The present study was designed to investigate the protective effect of glycyrrhizin on myocardial ischemia/reperfusion (I/R) injury through oxidative stress, inducible nitric oxide synthase (iNOS), and inflammatory reactions via high-mobility group box 1 (HMGB1) and mitogen-activated protein kinase (MAPK) expression. Sprague-Dawley rats were divided into five groups: Sham; myocardial I/R injury + non-treated; myocardial I/R injury + 2 mg/kg glycyrrhizin; myocardial I/R injury + 4 mg/kg glycyrrhizin; and myocardial I/R injury + 10 mg/kg glycyrrhizin. Pre-treatment with glycyrrhizin significantly reduced infarct size and inhibited creatine kinase, creatine kinase-MB, lactate dehydrogenase and cardiac troponin T activities in rats with myocardial I/R injury. Furthermore, glycyrrhizin treatment significantly suppressed oxidative stress, iNOS protein expression and inflammatory reactions in rats with myocardial I/R injury. Additionally, treatment with glycyrrhizin significantly decreased the release of HMGB1 from the cerebral cortex into the serum in rats with myocardial I/R injury. Notably, glycyrrhizin significantly suppressed p-ERK, p-p38 MAPK and p-c-Jun N-terminal kinase protein expressions, and promoted extracellular signal-regulated kinase protein expression in rats with myocardial I/R injury. Collectively, the present study indicates that the protective effect of glycyrrhizin may reduce myocardial I/R injury through oxidative stress, iNOS and inflammatory reactions, via HMGB1 and MAPK expression.