Protective effects of Zhenwutang on cardiac function in mice with uremic cardiomyopathy induced by subtotal nephrectomy
10.3969/j.issn.1673-4254.2015.12.12
- VernacularTitle:真武汤对大部分肾切除所致尿毒症心肌病小鼠心脏的保护作用
- Author:
Qi CHEN
1
;
Zhiliang LI
;
Bei LIU
;
Qiang FU
;
Quanneng YAN
Author Information
1. 南方医科大学珠江医院心血管内科
- Keywords:
Zhenwutang;
uremic cardiomyopathy;
AMPK-mTOR signal pathway
- From:
Journal of Southern Medical University
2015;(12):1725-1728
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effects of Zhenwutang (ZWT) on cardiac function in mice with uremic cardiomyopathy (UCM). Methods Thirty C57BL/6 mice were randomized into 3 equal groups, including a sham-operated group, subtotal nephrectomy (UCM model) group and subtotal nephrectomy with ZWT treatment group. The mice in the former two groups were treated with distilled water. The changes in cardiac functions, myocardial structure and renal function of the mice were evaluated with echocardiography, HE staining and biochemical assay, respectively. Western blotting was used to detect the expression level of adenosine monophosphate-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) in the heart tissues. Results Compared with the sham-operated group, the mice in the model group showed significantly lowered body weight and increased heart weight, heart index, left ventricular posterior wall thickness in diastole (LVPWd) and in systole (LVPWs), blood urea nitrogen (BUN) and serum creatinine (Scr) (P<0.05); Pathological examination revealed myocardial hypertrophy in the model group with markedly decreased expression levels of p-AMPK and significantly increased p-mTOR expression (P<0.05). ZWT treatment significantly decreased the heart weight, heart index, LVPWd, and LVPWs and expression level of p-mTOR (P<0.05), increased the expression level of p-AMPK (P<0.05), and obviously ameliorated histological injury of the heart in mice with UCM. Conclusion ZWT can protect the cardiac function in mice with subtotal nephrectomy-induced UCM possibly via the AMPK-mTOR signal pathway.
