Inhibitory Effect of PPARγ Agonist on the Proliferation of Human Pterygium Fibroblasts
Inhibitory Effect of PPARγ Agonist on the Proliferation of Human Pterygium Fibroblasts作者机构:Department of Ophthalmologythe First Clinical Medical Science College of China Three Gorges University Department of OphthalmologyUnion HospitalTongji Medical CollegeHuazhong University of Science and Technology
出 版 物:《Journal of Huazhong University of Science and Technology(Medical Sciences)》 (华中科技大学学报(医学英德文版))
年 卷 期:2010年第30卷第6期
页 面:809-814页
核心收录:
学科分类:1002[医学-临床医学] 100212[医学-眼科学] 10[医学]
基 金:supported by a grant from the Natural Sciences Foundation of Hubei Province China(No.2008CDA055)
主 题:DK2 peroxisome proliferator-activated receptor γ pterygium human pterygium fibroblasts proliferation inhibition
摘 要:The effects of DK2,a peroxisome proliferator-activated receptor γ agonist,on cultured human pterygium fibroblasts (HPFs) in virto were *** HPFs were incubated with 0-200 μmol/L DK2 for 12-72 *** MTT method was used to assay the bio-activity of DK2 at different doses and *** cytotoxic effect of DK2 was measured by LDH release *** cell cycle distribution and apoptosis were flow cytometrically *** expression of proliferating cell nuclear antigen (PCNA) in each group was detected by real-time PCR (RT-PCR) and Western *** results showed that administration of 1-75 μmol/L DK2 for 12-72 h could significantly inhibit HPF proliferation in a dose-and time-dependent ***2-treated cells did not release significant amount of LDH as compared with rosiglitazone-treated *** treatment with DK2 at concentrations of 15,25 μmol/L for 24 h,the number of HPFs in G 0 /G 1 phase was significantly increased while that in S phase was significantly decreased (P0.05),leading to arrest at G 0 /G 1 *** apoptosis rates of HPF cells in drug-treated groups were significantly higher than the rate of control group (P0.05).At the dosage range between 15-25 μmol/L,DK2 could inhibit the expression of PCNA mRNA and protein in HPFs in a dose-dependent fashion (P0.05).It was concluded that PPARγ agonist can significantly inhibit HPF proliferation,resulting in the arrest at G 0 /G 1 phase,induce the apoptosis of HPFs,and suppress the synthesis of PCNA,in dose-and time-dependent manners.