Pioglitazone Attenuates Vascular Fibrosis in Spontaneously Hypertensive RatsReport as inadecuate




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PPAR ResearchVolume 2012 2012, Article ID 856426, 7 pages

Research Article

Department of Cardiology, The Second Affiliated Hospital, Xi’an Jiaotong University School of Medicine, Shaanxi, Xi’an 710004, China

Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Xi’an Jiaotong University, Xi’an 710061, China

Department of Nuclear Medicine, The Second Affiliated Hospital, Xi’an Jiaotong University School of Medicine, Shaanxi, Xi’an 710004, China

Received 4 September 2011; Revised 23 November 2011; Accepted 19 January 2012

Academic Editor: Youfei Guan

Copyright © 2012 Dengfeng Gao 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

Objective. We sought to investigate whether the peroxisome proliferator-activated receptor-γ PPAR-γ ligand pioglitazone can attenuate vascular fibrosis in spontaneously hypertensive rats SHRs and explore the possible molecular mechanisms. Methods. SHRs 8-week-old males were randomly divided into 3 groups each for treatment: pioglitazone 10 mg-kg-day, hydralazine 25 mg-kg-day, or saline. Normal male Wistar Kyoto WKY rats served as normal controls. Twelve weeks later, we evaluated the effect of pioglitazone on vascular fibrosis by Masson’s trichrome and immunohistochemical staining of collagen III and real-time RT-PCR analysis of collagen I, III and fibronectin mRNA.Vascular expression of PPAR-γ and connective tissue growth factor CTGF and transforming growth factor-β TGF-β expression were evaluated by immunohistochemical staining, western blot analysis, and real-time RT-PCR. Results. Pioglitazone and hydralazine treatment significantly decreased systolic blood pressure in SHRs. Masson’s trichrome staining for collagen III and real-time RT-PCR analysis of collagen I, III and fibronectin mRNA indicated that pioglitazone significantly inhibited extracellular matrix production in the aorta. Compared with Wistar Kyoto rats, SHRs showed significantly increased vascular CTGF expression. Pioglitazone treatment significantly increased PPAR-γ expression and inhibited CTGF expression but had no effect on TGF-β expression. Conclusions. The results indicate that pioglitazone attenuated vascular fibrosis in SHRs by inhibiting CTGF expression in a TGF-β-independent mechanism.





Author: Dengfeng Gao, Ning Ning, Guanghua Hao, and Xiaolin Niu

Source: https://www.hindawi.com/



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