Rosiglitazone Inhibitory Effect on Mesangial Cell Proliferation and Extracellular Matrix Expression Induced by Angiotensin Ⅱ
- VernacularTitle:罗格列酮抑制血管紧张素Ⅱ诱导的肾小球系膜细胞增殖及细胞外基质表达
- Author:
yan, SUN
;
ai-hua, ZHANG
- Publication Type:Journal Article
- Keywords:
angiotensin Ⅱ;
mesangial cells;
peroxisome proliferator-activated receptor-?;
reactive oxygen species
- From:Journal of Applied Clinical Pediatrics
2006;0(23):-
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the inhibitory effect of peroxisome proliferator-activated receptor-?(PPAR?) agonist on mesangial cell(MC) proliferation and extracellular matrix expression induced by angiotensin Ⅱ(Ang Ⅱ).MethodsThe incorporation of 3H-thymidine(3H-TdR) and cell count were used as the measurement of MC proliferation.MC cell-cycle was analyzed by flow cytometry.Mouse primary MC was treated with various concentration of Ang Ⅱ(1,10,100 nmol/L) in the presence or Absence of N-acytosistin(NAC) or rosiglitazone.Transforming growth factor-?1(TGF-?1),plasminogen activator inhibitor-1(PAI-1),and fibronectin(FN) mRNA expression were determined by real time-PCR.Reactive oxygen species(ROS) production was measured by 2,7-dichlorofluorescein diacetate(DCFDA) fluorescence.Results1.One hundred nmol/L Ang Ⅱ increased 3H-TdR incorporation and cell number by 2.14 and 2.32 fold,respectively.Ang Ⅱ-induced MC proliferation was inhibited by PPAR? agonist rosiglitazone with dose-dependent manner in mouse MC.2.One hundred nmol/L Ang Ⅱ stimulation for 24 h induced 48% MC processed to S and G2/M phase.Rosiglitazone significantly blocked Ang Ⅱ increased cell number in S and G2/M phase.3.Rosiglitazone reduced Ang Ⅱ-induced TGF-?1,PAI-1,and FN mRNA expression with dose-dependent manner.4.One hundred nmol/L Ang Ⅱ stimulation for 60 min increased ROS production by 3.85 folds.Rosiglitazone significantly inhibited Ang Ⅱ-induced ROS production.Ten ?mol/L rosiglitazone almost completely blocked Ang Ⅱ-induced ROS production.ConclusionPPAR? agonist rosiglitazone could block Ang Ⅱ-induced MC proliferation and extracellular matrix expression via inhibition of ROS production.
