Carbon monoxide‑releasing molecules protect against blue light exposure and inflammation in retinal pigment epithelial cells
- Po‑Min Yang
- Kai‑Chun Cheng
- Shao‑Ho Yuan
- Being‑Sun Wung
Affiliations: Department of Ophthalmology, Chiayi Christian Hospital, Chiayi 60002, Taiwan, R.O.C., Department of Ophthalmology, Kaohsiung Municipal Hsiao‑kang Hospital, Kaohsiung 81267, Taiwan, R.O.C., Department of Microbiology, Immunology and Biopharmaceuticals, National Chiayi University, Chiayi 60002, Taiwan, R.O.C.
- Published online on: June 23, 2020 https://doi.org/10.3892/ijmm.2020.4656
Copyright: © Yang
et al. This is an open access article distributed under the
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The most common cause of vision loss among the elderly is age‑related macular degeneration (AMD). The aim of the present study was to investigate the potential cytoprotective and anti‑inflammatory effects of carbon monoxide‑releasing molecules (CORMs), and their ability to activate the expression of nuclear factor erythroid 2‑related factor 2 (Nrf2)‑related genes in human retinal pigment epithelium (RPE) cells, as well as the inhibition of endothelial cell migration. It was first determined that CORM2 and CORM3 suppressed blue light‑induced cell damage. In addition, a decrease in the level of cleaved poly(ADP‑ribose) polymerase 1 protein and dissipation of mitochondrial membrane potential were considered to reflect the anti‑apoptotic activity of CORMs. Furthermore, CORM2 induced Nrf‑2 activation and the expression of the Nrf2‑related genes heme oxygenase‑1 and glutamate‑cysteine ligase. Pretreatment with CORM2 abolished the blue light‑induced increase in oxidative stress, suggesting that CORM2‑induced antioxidant activity was involved in the cytoprotection against blue light. It was also demonstrated that CORMs markedly suppressed tumor necrosis factor (TNF)α‑induced intercellular adhesion molecule‑1 expression. Moreover, it was further observed that CORMs exert their inhibitory effects through blocking nuclear factor‑κB/p65 nuclear translocation and IκBα degradation in TNFα‑treated RPE cells. It was observed that CORM2, but not CORM3, protected against oxidative stress‑induced cell damage. CORMs abolished vascular endothelial growth factor‑induced migration of endothelial cells. The findings of the present study demonstrated the cytoprotective, antioxidant and anti‑inflammatory effects of CORMs on RPE cells and anti‑angiogenic effects on endothelial cells, suggesting the potential clinical application of CORMs as anti‑AMD agents.