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Galanthamine improves myocardial ischemia-reperfusion-induced cardiac dysfunction, endoplasmic reticulum stress-related apoptosis, and myocardial fibrosis by suppressing AMPK/Nrf2 pathway in rats

   
@article{ATM32301,
	author = {Xiaolin Hou and Minhuan Fu and Biao Cheng and Yu Kang and Dili Xie},
	title = {Galanthamine improves myocardial ischemia-reperfusion-induced  cardiac dysfunction, endoplasmic reticulum stress-related  apoptosis, and myocardial fibrosis by suppressing AMPK/Nrf2  pathway in rats},
	journal = {Annals of Translational Medicine},
	volume = {7},
	number = {22},
	year = {2019},
	keywords = {},
	abstract = {Background: Myocardial ischemia/reperfusion (I/R) injury is an important cause of myocardial infarction and heart failure after cardiovascular surgery. Galanthamine (Gal) is an important Amaryllidaceae alkaloid with anti-acetylcholinesterase and anti-inflammatory activity. The purpose of this study was to investigate the role of Gal in myocardial I/R injury.
Methods: In this study, an animal model of myocardial I/R injury was constructed, and the rats were divided into five groups (n=10): the sham, I/R model, I/R + Gal (1 mg/kg), I/R + Gal (3 mg/kg), and I/R + Aspirin (20 mg/kg) groups. The expression of related proteins was detected by Western blotting and Immunohistochemistry, and Histological lesion was detected by HE staining. 
Results: Results showed that Gal improves I/R—induced cardiac dysfunction in rats. Moreover, Gal inhibits I/R—induced endoplasmic reticulum stress (ERS)-related apoptosis by suppressing the expression of CHOP, Cleaved caspase 12, and caspase 3, and promoting the expression of CADD34 and BiP in rats. Furthermore, Gal mitigates I/R—induced myocardial fibrosis through restraining the expression of α-SMA and Collagen I in rats. Mechanically, Gal promoted the expression of AMPKα1, Nrf2 and HO-1. However, AMPK inhibitor Compound C exhibited the opposite effects. Collectively, this finding suggests that Gal improves I/R-induced cardiac dysfunction, ERS-related apoptosis, and myocardial fibrosis by activating AMPK/Nrf2 pathway in myocardial I/R rats. 
Conclusions: Given this evidence, Gal may be a potential therapeutic drug for the treatment of I/R injury.},
	issn = {2305-5847},	url = {https://atm.amegroups.org/article/view/32301}
}