The effect of valsartan on the expression of the receptor for advanced glycation end products in human glomerular mesangial cells.
- Author:
Lin-na ZHONG
1
;
Guo-liang HUANG
;
Min FENG
;
Ying ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II Type 1 Receptor Blockers; pharmacology; Antioxidants; pharmacology; Glycation End Products, Advanced; pharmacology; Humans; Mesangial Cells; cytology; metabolism; Oxidative Stress; drug effects; RNA, Messenger; genetics; metabolism; Receptor for Advanced Glycation End Products; Receptors, Immunologic; genetics; metabolism; Serum Albumin, Bovine; pharmacology; Tetrazoles; pharmacology; Valine; analogs & derivatives; pharmacology; Valsartan
- From: Chinese Journal of Applied Physiology 2011;27(3):338-342
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo elucidate the effect of valsartan on human glomerular mesangial cells oxidative stress and the expression of the receptor for advanced glycation end products (RAGE) induced by the advanced glycation end-products (AGEs).
METHODSHuman glomerular mesangial cells were treated with advanced glycation end-product-bovine serum albumin (AGE-BSA) in the presence of valsartan. The reactive oxygen species (ROS) in cells were measured by Flow cytometry, and the mRNA of p47 phox, which was the primary subunits of NADPH oxidase, was detected by semi-quantitative reberse transcription polymerase chain reaction (RT-PCR). The mRNA of RAGE was detected by RT-PCR and the RAGE protein was assayed by immunocytochemistry.
RESULTSThe product of ROS, and the expression of p47 phox and RAGE in mesangial cells, which were treated with AGE-BSA in the presence of valsartan, were down-regulated compared with the groups treated with AGE-BSA (P < 0.05). Valsartan dose-dependently and time-dependently inhibited the AGE-elicited overexpression of RAGE, ROS and p47(phox) in mesangial cells.
CONCLUSIONValsartan could inhibit RAGE expression through downregulation of oxidative stress.
