Effect and mechanism of Huangqi Shengmai Decoction in treatment of joint rat model of fatigue and myocardial injury.
10.19540/j.cnki.cjcmm.20220325.702
- Author:
Ya-Hui YUAN
1
;
Rong YUAN
1
;
Yu MIAO
1
;
Ya WANG
1
;
Peng-Qi LI
1
;
Jia-Qi HUI
1
;
Yu-Fan PAN
2
;
Zi-Han LI
2
;
Qi-Qi XIN
1
;
Wei-Hong CONG
1
Author Information
1. Laboratory of Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences Beijing 100091, China National Clinical Research Center for Chinese Medicine Cardiology Beijing 100091, China.
2. Laboratory of Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences Beijing 100091, China Tianjin University of Traditional Chinese Medicine Tianjin 301617, China.
- Publication Type:Journal Article
- Keywords:
Huangqi Shengmai Decoction;
autophagy;
fatigue;
mitochondria;
myocardial injury
- MeSH:
Rats;
Animals;
Ventricular Function, Left;
Rats, Sprague-Dawley;
Stroke Volume;
Diltiazem/pharmacology*;
Rats, Wistar;
Cardiomyopathies;
Heart Injuries;
Fibrosis;
Protein Kinases;
Ubiquitin-Protein Ligases
- From:
China Journal of Chinese Materia Medica
2022;47(19):5292-5298
- CountryChina
- Language:Chinese
-
Abstract:
This study aims to investigate the effects and the underlying mechanism of Huangqi Shengmai Decoction(HQSMD) in the treatment of fatigue and myocardial injury in a joint rat model. Wistar rats were assigned into 4 groups: sham, model, diltiazem hydrochloride(positive control), and HQSMD. The joint model of fatigue and myocardial injury was established by 14-day exhausted swimming followed by high ligation of the left anterior descending coronary artery. The rats in the sham group underwent a sham operation without coronary artery ligation or swimming. Since the fourth day after the ligation, swimming was continued in the model group and the drug-treated groups for the following 4 weeks. Meanwhile, the rats in the positive control group and the HQSMD group were respectively administrated intragastrically with diltiazem hydrochloride(20 mg·kg~(-1)·d~(-1)) and HQSMD(0.95 g·kg~(-1)·d~(-1)) for 4 weeks, while the shams and the models were given the same volume of normal saline. The left ventricular ejection fraction(LVEF), left ventricular fractional shortening(LVFS), grip strength, and myocardial pathophysiological changes were measured to evaluate the anti-fatigue and cardioprotective effects of HQSMD. The protein levels of PTEN-induced putative kinase 1(PINK1) and parkin in the myocardium were measured by Western blot to preliminarily elucidate the mechanism of HQSMD in ameliorating myocardial injury by suppressing mitochondrial autophagy. Compared with the shams, the models showed weakened heart function(LVEF and LVFS, P<0.01), decreased grasping ability(P<0.05), elevated blood urea nitrogen(BUN) and aldosterone(ALD) levels(P<0.01), aggravated myocardial fibrosis and connective tissue hyperplasia(P<0.01), and up-regulated protein levels of PINK1(P<0.01) and parkin(P<0.05). Four-week treatment with HQSMD increased the LVEF and LVFS levels(P<0.01), enhanced the grip strength(P<0.01), reduced the serum levels of BUN(P<0.01) and ALD(P<0.05), alleviated the pathological injury and fibrosis in the myocardium(P<0.01), and down-regulated the protein levels of PINK1(P<0.01) and parkin(P<0.05) in heart tissue. The results demonstrate that HQSMD may alleviate myocardial fibrosis and protect myocardium by suppressing the excessive mitochondrial auto-phagic activity and reducing the excessively elevated ALD level, thereby ameliorating fatigue and myocardial injury.
