Effect of peroxisome proliferator-activated receptor γ agonist on prostate epithelial cells
10.3760/cma.j.issn.1000-6702.2010.01.016
- VernacularTitle:过氧化物酶体增殖物激活受体γ激动剂对前列腺上皮细胞作用的研究
- Author:
Lanbin ZHENG
;
Yayuan ZHAO
;
Wei YU
;
Hui GUO
;
Jie JIN
- Publication Type:Journal Article
- Keywords:
Prostatic hyperplasia;
Cell line;
PPAR gamma;
Caspases;
Rosiglitazone
- From:
Chinese Journal of Urology
2010;31(1):52-55
- CountryChina
- Language:Chinese
-
Abstract:
Objective To assess the effect of peroxisome proliferator-activated receptor γ (PPARγ) agonist on prostate epithelial cells in vitro.Methods The expression of peroxisome proliferator-activated receptor γ(PPARγ) was studied by immunocytochemistry and immunofluorescence study.The RWPE-1 human prostate epithelial cell line was treated with PPARγ agonist rosiglitazone 100 μmol/L for 48 h.Analysis of apoptosis was performed by Caspase 3/7 activity assay.Mitochondria depolarization was measured by using the potential-sensitive color,JC-1.The expression of apoptosis-related proteins-Bax was investigated by immunohistochemistry.Results PPARγ mainly located in nucleus and perinucleus.RWPE-1 cell line treated with PPARγ agonist rosiglitazone showed higher Caspase 3/7 activity (10636±1032 RLU) than in control (5936±620 RLU),P<0.01 and significantly upregulated Bax level (8250±694 vs.6017±563)than in control group,P<0.01.In addition,mitochondrial membrane potential was depolarized in rosiglitazone treated cells.Conclusions PPARmay play important roles in the pathophysiology of BPH.The mechanism might be that PPARγ regulates cell apoptosis.It is suggested that the mitochondrial and Bax pathway might be involved in signaling PPARγ induced cell apoptosis.