Back to Search Start Over

Chronic Treatment With Qiliqiangxin Ameliorates Aortic Endothelial Cell Dysfunction in Diabetic Rats

Authors :
Fei Chen
Jia-Le Wu
Yun Mou
Shen-Jiang Hu
Guo-Sheng Fu
Source :
Journal of Cardiovascular Pharmacology and Therapeutics. 20:230-240
Publication Year :
2014
Publisher :
SAGE Publications, 2014.

Abstract

Qiliqiangxin (QL), a traditional Chinese medicine, has been shown to be beneficial for chronic heart failure. However, whether QL can also improve endothelial cell function in diabetic rats remains unknown. Here, we investigated the effect of QL treatment on endothelial dysfunction by comparing the effect of QL to that of benazepril (Ben) in diabetic Sprague-Dawley rats for 8 weeks. Cardiac function was evaluated by echocardiography and catheterization. Assays for acetylcholine-induced, endothelium-dependent relaxation (EDR), sodium nitroprusside-induced endothelium-independent relaxation, serum nitric oxide (NO), and nitric oxide synthase (NOS) as well as histological analyses were performed to assess endothelial function. Diabetic rats showed significantly inhibited cardiac function and EDR, decreased expression of serum NO and phosphorylation at Ser1177 on endothelial NOS (eNOS), and impaired endothelial integrity after 8 weeks. Chronic treatment for 8 weeks with either QL or Ben prevented the inhibition of cardiac function and EDR and the decrease in serum NO and eNOS phosphorylation caused by diabetes. Moreover, either QL or Ben suppressed inducible NOS (iNOS) protein levels as well as endothelial necrosis compared with the diabetic rats. Additionally, QL prevented the increase in angiotensin-converting enzyme 1 and angiotensin II receptor type 1 in diabetes. Thus, chronic administration of QL improved serum NO production, EDR, and endothelial integrity in diabetic rat aortas, possibly through balancing eNOS and iNOS activity and decreasing renin–angiotensin system expression.

Details

ISSN :
19404034 and 10742484
Volume :
20
Database :
OpenAIRE
Journal :
Journal of Cardiovascular Pharmacology and Therapeutics
Accession number :
edsair.doi.dedup.....b05f2a1839565484361f8e1deedaeee3
Full Text :
https://doi.org/10.1177/1074248414537705