安普克
内科学
内分泌学
脂联素
瘦素
蛋白激酶A
冠心病
心脏病学
联想(心理学)
医学
激酶
胰岛素抵抗
生物
细胞生物学
心理学
肥胖
心理治疗师
作者
JM Li,Wei Lü,Jianping Ye,Yiqun Han,H Chen,Wang Ls
出处
期刊:DOAJ: Directory of Open Access Journals - DOAJ
日期:2020-01-01
被引量:5
摘要
OBJECTIVE The aim of this study was to explore the association between the expression of adenosine monophosphate-activated protein kinase (AMPK) pathway and adiponectin (APN), leptin, and vascular endothelial function in rats with coronary heart disease (CHD). MATERIALS AND METHODS Experimental rats were divided into three groups, including: control (Col) group, CHD model (CHD) group, and CHD+AMPK activator (CHD+AICAR) group. Except those in Col group, all rats were fed with high-fat diet and intraperitoneally injected with pituitrin to establish the CHD model. The levels of serum APN, leptin, and endothelin-1 (ET-1) were determined via enzyme-linked immunosorbent assay (ELISA). The content of serum nitric oxide (NO) was detected using the nitrate reductase method. Meanwhile, the expression of AMPK pathway-related protein AMPKα in vascular endothelial tissues was detected via Western blotting (WB). Aortic vascular endothelial cells (VECs) were cultured with AICAR or ET-1 in vitro. Subsequently, the expressions of AMPK pathway and protein kinase B (AKT) pathway-related proteins were determined through co-immunoprecipitation and WB. Moreover, the expression level of NO in VECs was determined using the DAF-FM DA fluorescence probe. RESULTS Compared with Col group, CHD group showed significantly decreased levels of serum APN and NO (p<0.05), significantly increased the levels of leptin and ET-1 (p<0.05), as well as remarkably decreased protein expression of p-AMPKα in vascular endothelial tissues (p<0.05). After injection of AMPK activator AICAR (200 mg/kg), the protein expression of p-AMPKα in CHD rats was significantly activated (p<0.05). The levels of serum APN and NO were remarkably upregulated (p<0.05), while the levels of leptin and ET-1 were significantly reduced (p<0.05). Besides, AICAR could evidently activate the activity of AMPK pathway in VECs in vitro, upregulate the protein levels of p-eNOS (Ser1177) and p-AMPKα, and promote the secretion of NO (p<0.05). In addition, AICAR remarkably inhibited ET-1-induced expression of AKT pathway (p<0.05). CONCLUSIONS Activating the AMPK pathway may play a positive role in the normal function of VECs and exert a certain curative effect on CHD in rats.
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