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灵芝酸 A 通过调控 JAK2/STAT3/NF-κB 通路缓解大鼠心肌缺血再灌注损伤。

Ganoderic acid A alleviates myocardial ischemia-reperfusion injury in rats by regulating JAK2/STAT3/NF-κB pathway.

机构信息

Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.

Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.

出版信息

Int Immunopharmacol. 2020 Jul;84:106543. doi: 10.1016/j.intimp.2020.106543. Epub 2020 Apr 27.

Abstract

This study aimed to investigate the protective effect of GanodericacidA (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-κB signaling pathway-related proteins in myocardial tissue was measured by western blot. The results showed that the myocardial infarction extention 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-κB (NF-κB) 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-κB pathway.

摘要

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。通过结扎左前降支冠状动脉建立大鼠心肌损伤模型。我们测量了心脏血流动力学、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。进一步通过 Western blot 测定了心肌组织中 JAK2/STAT3/NF-κB 信号通路相关蛋白的表达。结果表明,GA 处理可明显减轻心肌梗死范围。与对照组相比,缺血再灌注大鼠的乳酸脱氢酶(LDH)和肌酸激酶(CK)明显升高,而 GA 组则明显降低。此外,GA 预处理可有效降低血清中炎症细胞因子的水平。再灌注组的 Janus 激酶 2(JAK2)、信号转导和转录激活因子 3(STAT3)和核因子-κB(NF-κB)的磷酸化水平明显高于对照组,而 GA 处理则逆转了这一现象。综上所述,GA 可能通过调节 JAK2/STAT3/NF-κB 通路减轻心肌损伤。

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