Potassium bromate-induced cell model of age-related macular degeneration in vitro
- Shu-Chun Kuo
- Yingxiao Li
- Kai-Chun Cheng
- Chia-Chen Hsu
- Juei-Tang Cheng
- Hui-Hsuan Lau
Affiliations: Department of Optometry, Chung Hwa University of Medical Technology, Tainan City 71701, Taiwan, R.O.C., Department of Nursing, Tzu Chi University of Science and Technology, Hualien City 97005, Taiwan, R.O.C., Department of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890, Japan, Graduate Institute of Gerontology and Health Care Management, Chang Gung University of Science and Technology, New Taipei City 11049, Taiwan, R.O.C., Department of Ophthalmology, Chi-Mei Medical Center, Tainan City 71003, Taiwan, R.O.C., Department of Obstetrics and Gynecology, Mackay Memorial Hospital, Taipei City 10449, Taiwan, R.O.C.
- Published online on: January 20, 2021 https://doi.org/10.3892/mmr.2021.11855
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Age‑related macular degeneration (AMD) progression occurs due to oxidative stress in retinal pigment epithelium (RPE) cells. To develop a new model of AMD, the present study investigated the effects of potassium bromate (KBrO3) on ARPE‑19 cells. Incubation with KBrO3 for 24 h significantly decreased ARPE‑19 cell viability in a concentration‑dependent manner compared with the control group. The MTT and lactate dehydrogenase assay results indicated that KBrO3 induced cell apoptosis. Compared with the control group, KBrO3 treatment significantly decreased the Bcl2/Bax ratio, as determined via western blotting, and caspase‑3 mRNA expression levels. Fluorescence microscopy indicated the increased ROS levels in cells treated with KBrO3. Endogenous antioxidant enzyme activities, including superoxide dismutase and glutathione peroxidase, were significantly inhibited by KBrO3 compared with the control group. Moreover, the antioxidants tiron and phloroglucinol inhibited KBrO3‑mediated effects on ARPE‑19 cells in a dose‑dependent manner. Additionally, GPR109A is the binding site of 4‑hydroxynonenal (4‑HNE). KBrO3 displayed cytotoxic effects in 293 cells, which naturally lack the GPR109A gene, but these effects were not observed in 4‑HNE‑treated 293 cells, suggesting that KBrO3 induced apoptosis without increasing endogenous 4‑HNE levels in cells. Moreover, the results suggested that KBrO3‑induced oxidative stress may activate STAT3 to increase VEGF expression in ARPE‑19 cells. Collectively, the results of the present study supported the potential use of KBrO3 to induce an in vitro model of AMD in ARPE‑19 cells.