心肌缺血再灌注损伤（I/R）与细胞凋亡密切相关。毛蕊异黄酮葡萄糖苷（CG）是黄芪的主要黄酮类成分之一，在大脑I/R过程中能够减轻I/R引起的神经元损伤。预实验表明，CG能够通过激活PI3K/Akt信号通路抑制心肌细胞凋亡，减轻心肌I/R。相关研究表明IL-10、JAK2/STAT3和PI3K/Akt信号通路在I/R的保护机制中发挥重要作用。因此，推测“CG是通过诱导IL-10调控JAK2/STAT3和PI3K/Akt信号通路减轻心肌I/R”。 本课题将在原有工作基础上构建Wistar大鼠I/R模型，应用STE评价CG对心肌功能的影响；探讨CG通过诱导IL-10调控JAK2/STAT3和PI3K/Akt信号通路，发挥抑制心肌细胞凋亡，减轻心肌I/R的作用和机制。目前，国内外未见相关报道。本课题的完成，将为急性心肌梗死的防治提供一种新思路、新靶点和新的技术平台，具有重要的理论意义和应用价值。

Myocardial Ischemia reperfusion injury is closely related with apoptosis. Calycosin-7-O-β-D-glucoside (CG), able to reduce neuron damage caused by I/R, is one of the main flavonoid ingredients of astragalus membranaceus. Early experiments indicated that CG could inhibit myocardial cell apoptosis through the activation of PI3K/Akt signaling pathway and eventually relieve myocardial Ischemia reperfusion injury. Related studies have shown that IL-10, JAK2/STAT3 and PI3K/Akt signaling pathway plays an important role in the protective mechanism of myocardial ischemia-reperfusion injury. Th1 inflammatory cytokines (IFN - gamma and IL - 2) and Th2 inflammatory cytokines (IL-4 and IL-10) were down-regulated and up-regulated, respectively, by astragalus membranaceus during its heart protection in autoimmune myocarditis. Several studies have shown that IL-10 can promote the activation of JAK2/STAT3 and PI3K/Akt signal pathway. To sum up, a hypothesis that myocardial ischemia-reperfusion injury alleviation of CG is developed by inducing IL-10 mediated activation of JAK2/STAT3 and PI3K/Akt signaling pathway was accordingly claimed. Based on the previous work, the present study built the model of myocardial ischemia-reperfusion injury of Wistar rat through coronary artery ligation, to explore the role of CG in its myocardial ischemia-reperfusion injury. Also, STE technology was used to evaluate effects of CG on myocardial function. Besides, anti-IL-10 antibody as well as JAK2 / STAT3, PI3K/Akt signaling pathway specific inhibitors was used to verify that CG realizes its important function, inhibiting myocardial apoptosis, by inducing IL-10 mediated activation of JAK2/STAT3 and PI3K/Akt signal pathway and thus protect myocardia from reperfusion injury. The present study will firstly report the protective mechanism of CG, which will be of important theoretical significance and application value and provide new thought, new targets and new technology for prevention and control of acute myocardial infarction (AMI).