Table of Contents
ISRN Endocrinology
Volume 2014 (2014), Article ID 601352, 7 pages
http://dx.doi.org/10.1155/2014/601352
Research Article

Pioglitazone Inhibits the Expressions of p22phox and p47phox in Rat Mesangial Cells In Vitro

Department of Endocrinology, Anhui Provincial Hospital Affiliated to Anhui Medical University, No. 17 Lujiang Road, Hefei 230001, China

Received 30 August 2013; Accepted 19 November 2013; Published 3 February 2014

Academic Editors: W. B. Chan and C. Fürnsinn

Copyright © 2014 Shan Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Aim. The purpose of this study was to investigate the effects of pioglitazone on oxidative stress and the expressions of p22phox and p47phox, subunits of NADPH oxidase, in mesangial cells (MCs). Method. Rat mesangial cells were cultured and randomly divided into normal glucose (NG) group, high glucose (HG) group, and pioglitazone group. After 48 h exposure, the supernatants and cells were collected. The expressions of p22phox and p47phox in MCs were detected by RT-PCR and western blot. The levels of intracellular ROS were determined by flow cytometry. Coloimetry method was used to detect malondialdehyde (MDA) concentrations and superoxide dismutase (SOD) activities. Results. Compared with the NG group, the expression levels of p22phox, p47phox and ROS significantly increased, the activity of SOD decreased in HG group, while the concentration of MDA greatly increased (). Pioglitazone significantly suppressed HG-induced p22phox and p47phox expressions and oxidative stress. The protein and gene expressions of p22phox and p47phox were markedly reduced after pioglitazone treatment, so did the ROS generation. The activities of SOD in MCs increased, while the concentrations of MDA in the supernatant decreased greatly by pioglitazone. Conclusions. Pioglitazone can inhibit HG-induced oxidative stress in MCs through suppressing p22phox and p47phox expressions.