International journal of ophthalmology · 2011
Troglitazone induced apoptosis of human pterygium fibroblasts through a mitochondrial-dependent pathway.
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Yang Xiao-Xi, Chen Jian, Zhou Qing, Guo Xian-Yin, Xiao Pan, Wu Jing, Xu Jin-Tang
Аннотация
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.
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.