Department of Rehabilitation Medicine, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou 510282, China.
Department of Cardiology Medicine, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou 510282, China.
Biomed Res Int. 2018 Aug 6;2018:1238175. doi: 10.1155/2018/1238175. eCollection 2018.
Electroacupuncture (EA) pretreatment plays a protective role in myocardial infarction injury. However, the mechanism of electroacupuncture remains unknown. The aim of this study was to confirm the protective effects of electroacupuncture (EA) on myocardial infarction injury and the possible mechanism.
Sprague-Dawley (SD) rats, used to serve as acute myocardial infarction (AMI) model, were divided into sham group, model (M) group, M+EA group, AMPK inhibitor Compound C (M+EA+CC), and AMPK inhibitor solvent control (M+EA+DMSO) group, respectively. Rats in EA group were pretreated with EA and those in M+EA+CC group with intravenous AMPK inhibitor Compound C. The myocardial morphological changes and infarct size were observed through HE staining and TTC staining, and the concentrations of CK-MB and LDH were detected using ELISA kits. Transmission electron microscopy was employed to observe the autophagosome formation, and the AMPK-dependent autophagy-related protein expression was detected by immunohistochemistry and western blot.
EA could alleviate myocardial infarction injury and decrease the concentrations of CK-MB and LDH. Transmission electron microscopy showed that EA could also regulate the AMPK-dependent autophagosome formation and the AMPK-dependent autophagy-related protein expression. AMPK inhibitor Compound C could impair the effect of EA through regulating the concentrations of CK-MB and LDH, autophagosome formation, and autophagy-related protein expression.
These results indicated that electroacupuncture could improve myocardial infarction injury and induce autophagy, and AMPK-dependent autophagy might be involved in this process.
电针预处理在心肌梗死损伤中发挥保护作用。然而,电针的机制尚不清楚。本研究旨在证实电针(EA)对心肌梗死损伤的保护作用及其可能的机制。
将 SD 大鼠用于急性心肌梗死(AMI)模型,分为假手术组、模型组(M 组)、M+EA 组、AMPK 抑制剂 Compound C(M+EA+CC)组和 AMPK 抑制剂溶剂对照(M+EA+DMSO)组。EA 组进行电针预处理,M+EA+CC 组进行静脉注射 AMPK 抑制剂 Compound C。通过 HE 染色和 TTC 染色观察心肌形态变化和梗死面积,ELISA 试剂盒检测 CK-MB 和 LDH 浓度。采用透射电镜观察自噬体形成,免疫组化和 Western blot 检测 AMPK 依赖性自噬相关蛋白表达。
EA 可减轻心肌梗死损伤,降低 CK-MB 和 LDH 浓度。透射电镜显示,EA 还可以调节 AMPK 依赖性自噬体形成和 AMPK 依赖性自噬相关蛋白表达。通过调节 CK-MB 和 LDH 浓度、自噬体形成和自噬相关蛋白表达,AMPK 抑制剂 Compound C 可损害 EA 的作用。
这些结果表明,电针可以改善心肌梗死损伤并诱导自噬,而 AMPK 依赖性自噬可能参与这一过程。