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Oxid Med Cell Longev. 2016;2016:9045736. doi: 10.1155/2016/9045736. Epub 2016 Dec 25.

Demethoxycurcumin Preserves Renovascular Function by Downregulating COX-2 Expression in Hypertension.

Author information

1
Department of Geriatrics, Zhongda Hospital, Medical School, Southeast University, 87# Ding Jiaqiao, Nanjing 210009, China.
2
Department of Physiology, Hebei Medical University, Shi Jiazhuang 050017, China.
3
Department of Neurology, Second Hospital of Hebei Medical University, Shi Jiazhuang 050017, China.

Abstract

Hypertension-associated endothelial dysfunction is largely due to the exaggerated vasoconstrictor generation by cyclooxygenase-2 (COX-2). COX-2 is induced under inflammatory condition. Demethoxycurcumin (DMC) is a major component of Curcuma longa L, which possesses anti-inflammatory action. This study aimed to examine whether DMC protects endothelial function in hypertension by modulating COX-2. Changes in isometric tension showed that in vivo and ex vivo treatment with DMC rescued the attenuated endothelium-dependent relaxations (EDRs) and elevated endothelium-dependent contractions (EDCs) in the renal arteries of SHR, which were also corrected by acute usage of the COX-2 inhibitor celecoxib. The restoration of renovascular activity by DMC was accompanied by the normalization of COX-2 expression. The enhanced COX-2 expression observed in the renal arteries of hypertensive patients was suppressed by incubation of excised arteries with DMC for 12 hrs. In the renal arteries of Wistar-Kyoto rats (WKY), DMC prevented the endothelial dysfunction caused by angiotensin II. The reduction in the generation of nitric oxide (NO) and expression of eNOS phosphorylation (Ser1177) in human umbilical vein endothelial cells caused by angiotensin II (Ang II) were restored by DMC or celecoxib. Our findings suggest that DMC may decrease COX-2 expression and improve endothelial function in hypertension.

PMID:
28105253
PMCID:
PMC5220467
DOI:
10.1155/2016/9045736
[Indexed for MEDLINE]
Free PMC Article

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