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首页> 外文期刊>International immunopharmacology >Ganoderic acid A alleviates myocardial ischemia-reperfusion injury in rats by regulating JAK2/STAT3/NF-kappa B pathway
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Ganoderic acid A alleviates myocardial ischemia-reperfusion injury in rats by regulating JAK2/STAT3/NF-kappa B pathway

机译:通过调节JAK2 / Stat3 / NF-Kappa B途径来减轻大鼠心肌缺血再灌注损伤的葡萄球菌

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摘要

This study aimed to investigate the protective effect of Ganoderic acid A (GA) on myocardial ischemia-reperfusion (MIR) injury. The myocardial injury model in rats was established by ligating left anterior descending coronary artery. We measured cardiac hemodynamic, antioxidant enzyme activity, and various biochemical indexes of myocardial tissue, and evaluated myocardial infarction and damage. Further, the expression of JAK2/STAT3/NF-kappa B signaling pathway-related proteins in myocardial tissue was measured by western blot. The results showed that the myocardial infarction extension was obviously reduced upon GA treatment. Compared with the control group, ischemia-reperfusion rats showed significant increase in lactate dehydrogenase (LDH) and creatine Kinase (CK), which were significantly decreased in GA group. Besides, GA pretreatment effectively decreased the levels of inflammatory cytokines in serum. The phosphorylation of Janus Kinase 2 (JAK2), signal transducer and activator of transcription (STAT3) and Nuclear factor-KB (NF-KB) in reperfusion group were significantly higher than that in control group, which were reversed upon GA treatment. In conclusion, GA may reduce myocardial injury by regulating JAK2/STAT3/NF-kappa B pathway.
机译:本研究旨在探讨灵芝酸A(GA)对心肌缺血再灌注(miR)损伤的保护作用。通过连接左前期下降冠状动脉来建立大鼠心肌损伤模型。我们测量了心肌动力学,抗氧化酶活性和心肌组织的各种生化指标,评估了心肌梗死和损伤。此外,通过蛋白质印迹测量心肌组织中JAK2 / Stat3 / NF-Kappa B信号传导途径相关蛋白的表达。结果表明,GA治疗后,心肌梗塞延伸明显降低。与对照组相比,缺血再灌注大鼠显示出乳酸脱氢酶(LDH)和肌酸激酶(CK)的显着增加,在GA组中显着降低。此外,GA预处理有效地降低了血清中炎性细胞因子的水平。再灌注组的Janus激酶2(JAK2),转录(STAT3)和核因子-KB(NF-KB)的磷酸化显着高于对照组的磷酸盐,其在GA处理时逆转。总之,GA通过调节JAK2 / Stat3 / NF-Kappa B途径来减少心肌损伤。

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