The effects of salidroside on the apoptosis pathway of myocardial cells in acute exhausted rats.
10.12047/j.cjap.5691.2019.080
- Author:
Tao QIE
1
;
Peng XU
2
;
Bing-Xin ZHANG
3
;
Xue-Bin CAO
2
Author Information
1. Emergency Department, the 1st Central Hospital of Baoding, Baoding 071000.
2. Department of Cardiology, the Hospital of the 82nd Group Army, Baoding 071000.
3. Pathology Department, the 1st Central Hospital of Baoding, Baoding 071000, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Biomarkers;
blood;
Fatigue;
physiopathology;
Female;
Glucosides;
pharmacology;
Heart;
drug effects;
Male;
Myocardial Ischemia;
drug therapy;
Myocardium;
cytology;
Phenols;
pharmacology;
Physical Conditioning, Animal;
Rats;
Rats, Sprague-Dawley
- From:
Chinese Journal of Applied Physiology
2019;35(4):376-380
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate whether salidroside (Sal) plays a part in protecting myocardial cell through reducing the myocardial ischemia and the apoptosis pathway of both death receptors and mitochondria in acute exhausted rats.
METHODS:Male SD rats were randomly divided into 4 groups (n=6): control group(Con), acute exhaustive swimming group (EE), low-dose and high-dose Sal pre-treatment exhaustive swimming group (SLE, SHE). Rats were treated with Sal solution (15 or 30 mg/(kg·d)) or 0.9%NaCl (3 ml/(kg·d)) by intraperitoneal injection for 15 d, respectively. The Con group did not carry out swimming training. The next day after the end of intraperitoneal administration, the rats in EE, SLE and SHE group were forced to swim until they were exhausted followed the standard of Thomas. After the end of exhaustive exercise, the rats were anesthetized and the blood samples and hearts were collected immediately. The myocardial ischemia and hypoxia area and myocardial apoptosis index (AI) were also observed. Serum ischemia modified albumin (IMA), cardiac troponin I (cTnI), brain natriuretic peptide(BNP) and myocardial cell Bcl-2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2) were determined. The expressions of myocardial TNF receptor superfamily member 6 (Fas), cytochrome C (Cyto-c), aspartate proteolytic enzyme-3(Caspase-3), aspartate proteolytic enzyme-8(Caspase-8), and aspartate proteolytic enzyme-9(Caspase-9) were detected.
RESULTS:Compared with the Con group, the myocardial ischemia and hypoxia area in EE group was increased significantly. The serum levels of IMA, cTnI and BNP, AI and Bax levels and cardiac Fas, Cyto-C, Caspase-3, Caspase-8 and Caspase-9 protein expressions of EE group were also increased significantly (P＜0.01), while the protein expression of Bcl-2 in cardiac tissues was decreased significantly (P＜0.01). Compared with the EE group, the myocardial ischemia and hypoxia area, serum levels of IMA, cTnI and BNP, AI and Bax levels, and the protein expressions of cardiac Fas, Cyto-C, Caspase-3, Caspase-8 and Caspase-9 in Sal group were all decreased significantly(P＜0.01). while the protein expression of cardiac Bcl-2 in Sal group were increased significantly (P＜0.01).
CONCLUSION:Sal plays a role in protecting myocardial cell through reducing the myocardial ischemia and inhibiting myocardial cell apoptosis in exhaustive exercise rats. The mechanism of reducing myocardial cell apoptosis may be related to inhibiting the expressions of Fas, Cyto-C, Caspase-3, Caspase-8, Caspase-9 and increasing the expression of Bcl-2.
