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Troglitazone induced apoptosis of human pterygium fibroblasts through a mitochondrial-dependent pathway

Xiao-Xi Yang1, Jian Chen, Qing Zhou

  • 1Department of Ophthalmology, the First Affiliated Hospital of Jinan University, Guangzhou 510632, Guangdong Province, China.

International Journal of Ophthalmology
|May 4, 2012
PubMed
Abstract

Insights

Troglitazone induces apoptosis in human pterygium fibroblasts (HPF) by disrupting mitochondrial function. This study reveals a potential therapeutic pathway for pterygium treatment.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Pharmacology

Background:

  • Pterygium is a proliferative fibrovascular condition affecting the conjunctiva.
  • Understanding the cellular mechanisms of pterygium is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the effects of troglitazone on human pterygium fibroblasts (HPF).
  • To elucidate the mechanism by which troglitazone affects HPF viability and apoptosis.

Main Methods:

  • Cell viability was assessed using cell counting kit-8.
  • Apoptosis was quantified via AnnexinV-FITC/PI staining, caspase activity assays, and Western blotting.
  • Mitochondrial membrane potential was analyzed using flow cytometry.

Main Results:

  • Troglitazone demonstrated a dose-dependent inhibition of HPF cell survival.
  • The drug induced apoptosis, characterized by altered mitochondrial potential and increased Bax/Bcl-2 ratio.
  • Peroxisome proliferator-activated receptor γ (PPAR-γ) was expressed in pterygium tissues.

Conclusions:

  • Troglitazone induces apoptosis in human pterygium fibroblasts.
  • The mechanism involves a mitochondrial-dependent pathway, suggesting a potential therapeutic role for troglitazone in pterygium.
Keywords:
apoptosisperoxisome proliferator-activated receptor γpterygiumtroglitazone

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