Abstract
Background 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. Methods 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. Results 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. Conclusion These results indicated that electroacupuncture could improve myocardial infarction injury and induce autophagy, and AMPK-dependent autophagy might be involved in this process.
Highlights
Myocardial infarction resulting from coronary arterial occlusion leads to myocardial necrosis, contractile dysfunction, arrhythmias, and even heart failure; ischemic heart disease is the major cause of mortality worldwide [1]
In the model group the myocardial cells were loosely connected and some were in disarray, with interstitial inflammatory exudation being significantly increased
The results indicated that the acute myocardial infarction (AMI) model was successfully established; EA treatment could alleviate myocardial infarction; and AMPK pathway was involved in the regulatory process of EA
Summary
Myocardial infarction resulting from coronary arterial occlusion leads to myocardial necrosis, contractile dysfunction, arrhythmias, and even heart failure; ischemic heart disease is the major cause of mortality worldwide [1]. Electroacupuncture (EA) pretreatment plays a protective role in myocardial infarction injury. The aim of this study was to confirm the protective effects of electroacupuncture (EA) on myocardial infarction injury and the possible mechanism. Transmission electron microscopy was employed to observe the autophagosome formation, and the AMPKdependent autophagy-related protein expression was detected by immunohistochemistry and western blot. Transmission electron microscopy showed that EA could 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 CKMB 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
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