Effects of astaxanthin on antioxidant parameters in ARPE-19 cells on oxidative stress model
| Autor: | Yiğit Musa, Güneş Alime, Uğuz Cihangir, Yalçın Tök Özlem, Tök Levent, Öz Ahmi, Nazıroğlu Mustafa |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: | |
| Zdroj: | International Journal of Ophthalmology, Vol 12, Iss 6, Pp 930-935 (2019) |
| Druh dokumentu: | article |
| ISSN: | 2222-3959 2227-4898 |
| DOI: | 10.18240/ijo.2019.06.08 |
| Popis: | AIM: To observe the protective effect of astaxanthin (AST) against hydroquinone (HQ) mediated cell death in the apoptotic cascade and evaluate intracellular Ca2+ release, caspase-3, and -9 activation, reactive oxygen species (ROS) production in ARPE-19 cells. METHODS: We cultured ARPE-19 cells in special mediums and performed MTT tests to determine protective effect of AST, before exposing the cells to HQ in an incubator. We analyzed intracellular Ca2+ release experiments, mitochondrial membrane depolarization, glutathione (GSH), glutathione peroxidase (GSH-Px) and ROS experiments, and apoptosis assay. RESULTS: ROS production ranges depend on the amount of cell death. We computed the correlation between ROS ranges and cell death by 20,70-dichlorofluorescein fluorescence, and Ca2+ levels by Fura-2-AM. HQ-induced cell death found out to rise ranges of caspase-3 and -9, and mitochondrial depolarization. These three steps were delayed by AST management. CONCLUSION: ARPE-19 cells are avoided from HQ-induced ROS production and caspase-3 and -9 activation by AST. AST may limit the range of caspase synthesis, Ca2+ release and excess production of ROS with antiapoptotic effect. This study proposes a new therapeutic approach for the treatment of age-related macular degeneration. |
| Databáze: | Directory of Open Access Journals |
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