中文摘要：

·AIM:To study the effect of troglitazone on primary culture human pterygium fibroblasts (HPF).·METHODS:Cell viability loss and apoptosis were quantified by cell counting kit-8,AnnexinV-FITC/PI double staining,caspases activity test and western blotting.Flow cytometry was used to detect mitochondrial membrane potential.·RESULTS:Peroxisome proliferator-activated receptor γ (PPAR-γ) was positively expressed in pterygium specimens (n=5).Troglitazone showed dose-dependent inhibition of cell survival,induced phospholipids redistribution,activated caspase-3,-9,and altered mitochondrial potential.Western blot assay demonstrated the increase of Bax/Bcl-2 protein ratio.·CONCLUSION:Troglitazone induced apoptosis of HPF through a mitochondrial-dependent pathway.·

英文摘要：

AIM: To study the effect of troglitazone on primary culture human pterygium fibroblast (HPF). METHODS: Cell viability loss and apoptosis were quantified by cell counting kit-8, AnnexinV-FITC/PI double staining, caspases activity test and western blotting. Flow cytonnetry was used to detect mitochondrial membrane potential. RESULTS: Peroxisome proliferator-activated receptor gamma (PPAR-gamma) was positively expressed in pterygium specimens (n = 5). Troglitazone showed dose-dependent inhibition of cell survival, induced phospholipids redistribution, activated caspase-3, -9, and altered mitochondrial potential. Western blot assay demonstrated the increase of Bax/Bcl-2 protein ratio. CONCLUSION: Troglitazone induced apoptosis of HPF through a mitochondrial-dependent pathway.