Calycosin-7-O-β-d-glucoside attenuates myocardial ischemia-reperfusion injury by activating JAK2/STAT3 signaling pathway via the regulation of IL-10 secretion in mice
Calycosin-7-O-β-d-glucoside attenuates myocardial ischemia-reperfusion injury by activating JAK2/STAT3 signaling pathway via the regulation of IL-10 secretion in mice
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毛蕊花苷-7-O-β-d-葡萄糖苷通过调节IL-10分泌激活JAK2/STAT3信号通路减轻心肌缺血再灌注损伤
DOI：
10.1007/s11010-019-03639-z
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发表时间：
2019-11-11
影响因子：
4.3
通讯作者：
Ren, Min
中科院分区：
文献类型：
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作者：
Liu, Yujie;Che, Guoying;Ren, Min
毛蕊异黄酮-7-O-β-D-葡萄糖苷（CG）是黄芪的主要成分，本研究旨在探讨CG是否通过调节IL-10/JAK 2/STAT 3信号通路对心肌缺血再灌注损伤具有保护作用。H9 C2细胞经I/R处理后，用1 μ mCG预处理。结扎冠状动脉左前降支（LAD）建立小鼠心肌I/R损伤模型，I/R前静脉注射CG 30 mg/kg。体外和体内实验结果表明，CG上调IL-10水平，激活JAK 2/STAT 3通路，保护心肌细胞免受I/R诱导的细胞凋亡。在体血流动力学测定、TTC染色、TUNEL染色和western blot结果表明，CG对心肌功能和细胞凋亡的保护作用均被IL-10 R α中和抗体逆转。CG诱导的JAK 2/STAT 3信号通路的磷酸化激活也被IL-10的阻断所抑制。综上所述，CG可能通过上调IL-10的分泌，激活JAK 2/STAT 3信号通路，从而减轻心肌I/R损伤，这为我们深入了解CG对心肌I/R损伤的保护作用机制提供了新的思路。
Calycosin-7-O-beta-d-glucoside (CG) is the component of Astragali Radix, and the aim of the present study is to investigate whether CG protects myocardium from I/R-induced damage by the regulation of IL-10/JAK2/STAT3 signaling pathway. H9C2 cells were subjected to I/R treatment and pretreated with 1 mu m CG in vitro. In addition, a mouse model of myocardial I/R injury was induced by left anterior descending (LAD) coronary artery ligation and administrated with 30 mg/kg CG by intravenous injection before I/R surgery. In vitro and in vivo results showed that CG up-regulated IL-10 level, activated the JAK2/STAT3 pathway, and protected myocardial cells from I/R-induced apoptosis. The hemodynamic measurement, TTC staining, TUNEL staining, and western blot results in vivo showed that the protective effects of CG on myocardial function and cell apoptosis were all reversed by the IL-10R alpha neutralizing antibody. CG-induced phosphorylation activation of JAK2/STAT3 signaling pathway was also suppressed by the blocking of IL-10. In summary, these findings suggest that CG might alleviate myocardial I/R injury by activating the JAK2/STAT3 signaling pathway via up-regulation of IL-10 secretion, which provides us insights into the mechanism underlying the protective effect of CG on myocardial I/R injury.