title: The effects of alpha lipoic acid in preventing oxidative stress-induced retinal pigment epithelial cell injury.
abstract: This study evaluated the protective effect of alpha lipoic acid (ALA) in human adult retinal pigment epithelium cells (ARPE-19). An RPE oxidative stress model was established in ARPE-19 cells. Cell apoptosis was detected by Annexin V/PI staining and Hoechst33342 staining. Autophagy activation was evaluated by formation of acidic vesicular organelles (AVO) as well as protein expression of Atg5 and LC3. Akt phosphorylation and Bax protein expression were measured using western blot. Exogenous H2O2 significantly increased intracellular ROS concentration and decreased the viability of ARPE-19 cells in a dose-dependent way. H2O2 (12.5 μmol/L) induced early stage apoptosis, significantly decreased Akt phosphorylation, and increased Bax protein level 4 h after stimulation. H2O2 (12.5 μmol/L) significantly increased AVO formation, mRNA and protein levels of Atg-5, and protein expression of LC3 I and II. Treatment of ARPE-19 cells with 37.5 μmol/L ALA significantly blocked increased intracellular ROS level, apoptosis, AVO formation, as well as elevation of Atg5, LC3 I, and II protein levels induced by 12.5 μmol/L H2O2. Exogenous H2O2 induces apoptosis and activation of autophagy in human adult retinal pigment epithelium cells through Akt-Bax signaling. ALA is effective in protecting RPE cells from H2O2-induced cell death.
authors.affiliation: a Department of Ophthalmology and Visual Sciences, the 2nd Xiangya Hospital, Central South University, 410011, Changsha, Hunan, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Li
authors.forename: Hongwei
authors.initials: H
authors.lastname: Shen
authors.forename: Jingming
authors.initials: J
authors.lastname: Shi
authors.forename: Luosheng
authors.initials: L
authors.lastname: Tang
mesh_terms: D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001343:Autophagy / Q000187:drug effects; D002460:Cell Line; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D051058:Oncogene Protein v-akt / Q000378:metabolism; D016877:Oxidants / Q000494:pharmacology; D018384:Oxidative Stress; D010766:Phosphorylation; D055213:Retinal Pigment Epithelium / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction; D008063:Thioctic Acid / Q000494:pharmacology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000975:Antioxidants; C477012:MAP1LC3A protein, human; D008869:Microtubule-Associated Proteins; D016877:Oxidants; D051028:bcl-2-Associated X Protein; D008063:Thioctic Acid; D006861:Hydrogen Peroxide; D051058:Oncogene Protein v-akt
keywords: ARPE-19; Akt; Bax; apoptose; apoptosis; autophagie; autophagy