首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >Calycosin-7-O-beta-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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Calycosin-7-O-beta-d-glucoside attenuates myocardial ischemia-reperfusion injury by activating JAK2/STAT3 signaling pathway via the regulation of IL-10 secretion in mice

机译:通过在小鼠中调节IL-10分泌物,通过激活JAK2 / Stat3信号通路来衰减心肌缺血再灌注损伤的心肌缺血性损伤

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摘要

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.
机译:Calycosin-7-O-Beta-D-葡萄糖苷(CG)是黄芪基的组成部分,目前研究的目的是通过IL-10的调节研究CG是否保护心肌免受I / R诱导的损伤。 JAK2 / Stat3信令路径。将H9C2细胞进行I / R处理,并在体外用1μmcg预处理。此外,通过左前期下降(LAD)冠状动脉连接诱导和通过静脉注射在I / R手术前施用30mg / kg CG诱导小鼠模型。体外和体内结果表明,CG上调IL-10水平,激活JAK2 / Stat3途径,并受到I / R诱导的细胞凋亡的保护性心肌细胞。体内血液动力学测量,TTC染色,TUREL染色和Western印迹结果表明,CG对心肌功能和细胞凋亡的保护作用全部由IL-10Rα中和抗体反转。 CG诱导的JAK2 / Stat3信号传导途径的磷酸化活化也被IL-10的阻断抑制。总之,这些研究结果表明,CG可以通过激活jak2 / stat3信号传导途径来通过对IL-10分泌的上调激活jak2 / stat3信号通路来减轻心肌I / r损伤,这为我们提供了对CG对心肌I / CG保护作用的机制的洞察力。伤害伤害。

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