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Author Huang, Guo-Zhi ♦ Wang, Xian-Bao ♦ Lin, Hong-Xin ♦ He, Shang-Fei ♦ Zeng, Qing ♦ Zhou, Yu-Qing ♦ Tan, Zhi-Peng ♦ He, He
Source Directory of Open Access Journals (DOAJ)
Content type Text
Publisher Hindawi Limited
File Format HTM / HTML
Date Created 2018-08-19
Copyright Year ©2018
Language English
Subject Domain (in LCC) R
Subject Keyword Medicine
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.
ISSN 23146133
Age Range 18 to 22 years ♦ above 22 year
Educational Use Research
Education Level UG and PG ♦ Career/Technical Study
Learning Resource Type Article
Publisher Date 2018-01-01
e-ISSN 23146133
Journal BioMed Research International
Volume Number 2018


Source: Directory of Open Access Journals (DOAJ)