Aucubin protects cardiomyocytes from apoptosis by activating ERß pathway
10.3969/j.issn.1001-1978.2021.01.012
- Author:
Chun-Xiao LI
1
;
Lu-Sha ZHANG
1
;
Li-Yuan ZHANG
1
;
Lu-Lu MA
1
;
Qian-Yi WANG
1
;
Le-Yu FANG
1
;
Wen-Jie YANG
1
;
Wei SUN
1
;
Yu-Ze LENG
1
;
Lu CHEN
1
;
Hong WANG
1
Author Information
1. School of Integrative Medicine, Key Lab of Pharmacology of Traditional Chinese Medical Formulae, Ministry of Education, Tianjin Key Lab of Chinese Medicine Pharmacology, Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Aucubin;
Cardiomyocyte;
Estrogen receptor;
Phytoestrogens;
Tumor necrosis factor-a
- From:
Chinese Pharmacological Bulletin
2021;37(1):68-74
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the effect of aucubin aucubin (AU), one of the effective ingredients of eucommia, plantain, rehmannia and other herbs, on cardiomyocyte apoptosis and cardiac function after acute myocardial infarction (MI) and the possible mechanisms. Methods In this study, the mouse models of MI were established by ligation of the anterior descending branch of the left coronary artery. Left ventricular function and the infarct size were detected using echocardiography and Masson staining. A Tumor necrosis factor-a (TNF-ot)/cycloheximide (C H X) model of cardiomyocyte injury was established, and the effects AU on myocardial injury were examined using IncuCyte live cell imaging, Western blot and TUNEL staining. Results AU administration dramatically improved cardiac function recovery and decreased infarct size after MI. AU inhibited the apoptosis of cardiomyocytes, reduced the expressions of caspase-3, and significantly increased the ratio of Bcl-2/Bax induced by TNF-ot/ CHX. Meanwhile, the estrogen receptor ß (ERß) protein level was elevated by AU, and the antiapoptotic effect of AU was blocked by ERß inhibitor. Conclusions AU can alleviate MI injury and improve cardiac function via inhibiting the apoptosis of cardiomyocytes, and its mechanism is the activation of ERß pathway.
