目的 探究金合欢素调节生长停滞特异性蛋白6（GAS6）/Axl受体酪氨酸激酶（Axl）信号通路对慢性心力衰竭大鼠心肌损伤的影响。方法 采用ip阿霉素的方法构建慢性心力衰竭大鼠模型，将大鼠随机分为对照组、模型组、金合欢素（5、10、20 mg/kg）组、卡托普利（100 mg/kg）组、金合欢素＋R428（20 mg/kg金合欢素＋75 mg/kg GAS6/Axl信号通路抑制剂R428）组，每组12只。心脏超声检测大鼠心功能指标；生化仪检测大鼠心肌损伤指标；ELISA检测大鼠心力衰竭指标；HE染色观察心肌组织病理变化；TUNEL检测心肌组织细胞凋亡；Western blotting检测GAS6/Axl信号通路相关蛋白表达。结果 金合欢素各剂量组、卡托普利组较模型组心肌细胞损伤程度依次得到改善；相较于金合欢素20 mg/kg组，金合欢素＋R428组心肌细胞损伤程度有所加剧。相比于模型组，金合欢素各剂量组、卡托普利组FS、LVEF、GAS6蛋白表达、p-Axl/Axl值升高，LVDs、LVDd、cTnT、cTnI、CK-MB、NT-proBNP水平，心肌细胞凋亡率降低（P＜0.05）；相比于金合欢素20 mg/kg组，金合欢素＋R428组FS、LVEF、GAS6蛋白表达及p-Axl/Axl值降低，LVDs、LVDd、cTnT、cTnI、CK-MB、NT-proBNP水平及心肌细胞凋亡率升高（P＜0.05）。结论 金合欢素可能通过激活GAS6/Axl信号通路减轻慢性心力衰竭大鼠心肌损伤。

Objective To explore the effect of acacetin on myocardial injury in rats with chronic heart failure by regulating the GAS6/Axl signaling pathway. Methods The rat model of chronic heart failure was constructed by the method of ip doxorubicin. Rats were randomly divided into the control group, the model group, the acacetin (5, 10, 20 mg/kg) group, the captopril (100 mg/kg) group, and the acacetin +R428 (20 mg/kg acacetin + 75 mg/kg GAS6/Axl signaling pathway inhibitor R428) group, with 12 rats in each group. Cardiac ultrasound was used to detect cardiac function indicators in rats. The biochemical analyzer was performed to measure indicators of myocardial injury in rats. ELISA was performed to detect indicators of heart failure in rats. HE staining was conducted to assess pathological alterations in myocardial tissues. TUNEL was used to measure apoptosis of myocardial tissue cells. Western blotting was utilized to assess proteins involved in the GAS6/Axl signaling axis. Results The degree of myocardial cell injury in each dose group of acacetin and the captopril group was improved successively compared with the model group. Compared with the acacetin 20 mg/kg group, the degree of myocardial cell damage in the acacetin + R428 group was exacerbated. Compared with the model group, FS, LVEF, GAS6 protein, p-Axl/Axl ratio were increased, but LVDs, LVDd, cTnT, cTnI, CK-MB, NT-proBNP, and myocardial cell apoptosis rate werer decreased in the acacetin group and captopril group (P<0.05). Compared with the acacetin 20 mg/kg group, FS, LVEF, GAS6 protein, p-Axl/Axl ratio were decreased, LVDs, LVDd, cTnT, cTnI, CK-MB, NT-proBNP, and myocardial cell apoptosis rate were increased in the acacetin + R428 group (P<0.05). Conclusion Acacetin may alleviate myocardial injury in rats with chronic heart failure by activating the GAS6/Axl signaling pathway.

R285.5;R286.2

北京市科技计划课题（Z221100007422106）