Arginase inhibition restores endothelial function in diet-induced obesity
- Authors
- Chung, Ji Hyung; Moon, Jiyoung; Lee, Youn Sue; Chung, Hye-Kyung; Lee, Seung-Min; Shin, Min-Jeong
- Issue Date
- 22-8월-2014
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Arginase; Endothelial function; Nitric oxide; Obesity
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.451, no.2, pp.179 - 183
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 451
- Number
- 2
- Start Page
- 179
- End Page
- 183
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/97666
- DOI
- 10.1016/j.bbrc.2014.07.083
- ISSN
- 0006-291X
- Abstract
- Arginase may play a major role in the regulation of vascular function in various cardiovascular disorders by impairing nitric oxide (NO) production. In the current study, we investigated whether supplementation of the arginase inhibitor N-omega-hydroxy-nor-L-arginine (nor-NOHA) could restore endothelial function in an animal model of diet-induced obesity. Arginase 1 expression was significantly lower in the aorta of C57BL/6J mice fed a high-fat diet (HFD) supplemented with nor-NOHA (40 mg kg(-1)/day) than in mice fed HFD without nor-NOHA. Arginase inhibition led to considerable increases in eNOS expression and NO levels and significant decreases in the levels of circulating ICAM-1. These findings were further confirmed by the results of siRNA-mediated knockdown of Arg in human umbilical vein endothelial cells. In conclusion, arginase inhibition can help restore dysregulated endothelial function by increasing the eNOS-dependent NO production in the endothelium, indicating that arginase could be a therapeutic target for correcting obesity-induced vascular endothelial dysfunction. (C) 2014 Elsevier Inc. All rights reserved.
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