目的 检测丹皮酚（paeonol）对大鼠心梗后心肌重构和心脏功能的改善作用并探究其作用机制。方法 采用SD大鼠和人心肌细胞H9C2分别建立体内心肌梗死动物模型和体外心肌细胞缺氧细胞模型。Western blot检测Pink1、Parkin、LC3Ⅰ、LC3Ⅱ、Beclin-1和Mfn2的表达水平。本研究通过ELISA试剂盒检测心肌损伤标志物乳酸脱氢酶（LDH）和肌酸激酶同工酶（CK-MB）在血浆中的含量。细胞凋亡率采用TUNEL检测。使用超声心动图和生物机能采集系统检测大鼠心脏功能和心室重构情况。结果 丹皮酚减少了心肌损伤标志物LDH和CK-MB的释放，并减弱了H9C2细胞凋亡。丹皮酚激活了Pink1/Parkin信号通路，并因此增强了线粒体自噬。进一步的研究表明，丹皮酚显著减轻了SD大鼠心梗后心室重构情况并改善了心脏功能。结论 丹皮酚通过激活Pink1/Parkin信号通路促进线粒体自噬，进而减轻了心肌细胞损伤，改善了大鼠心脏功能和心室重构情况。

Objective This research aimed to investigate effects of paeonol on myocardial infarction and explore the underlying mechanism.Methods SD rats and H9C2 cells were used to establish myocardial infarction animal model and cell model. Western blot was performed to determine the expression level of Pink1, Parkin, LC3Ⅰ、LC3Ⅱ、Beclin-1 and Mfn2. Myocardial injury markers LDH and CK were detected by ELISA kits. H9C2 apoptosis was detected by TUNEL. Left ventricular functions and ventricular remodeling were analyzed by echocardiography.Results Paeonol reduced H9C2 apoptosis as well as LDH and CK release. Paeonol activated Pink1/Parkin pathway and promoted mitophagy protein expression. Furthermore, Paeonol improved ventricular functions and ventricular remodeling after myocardial infarction.Conclusion Paeonol promotes mitophagy by activating Pink/Parkin signaling pathway and improves ventricular functions and ventricular remodeling.

河北省卫生计生委办公室，河北省医学科学研究重点课题计划（编号：20181153）：丹皮酚通过Pink1/Parkin 通路调控细胞自噬抑制心梗后心室重构，负责人：刘超。