Selenium Protects ARPE-19 and ACBRI 181 Cells against High Glucose-Induced Oxidative Stress

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dc.authoridUğuz, A. Cihangir/0000-0002-5778-581X
dc.contributor.authorBardak, Handan
dc.contributor.authorUguz, Abduelhadi Cihangir
dc.contributor.authorBardak, Yavuz
dc.contributor.authorRocha-Pimienta, Javier
dc.contributor.authorDelgado-Adamez, Jonathan
dc.contributor.authorEspino, Javier
dc.date.accessioned2024-01-22T12:22:26Z
dc.date.available2024-01-22T12:22:26Z
dc.date.issued2023
dc.departmentKMÜen_US
dc.description.abstractDiabetic retinopathy (DR), a complication of diabetes mellitus (DM), can cause severe visual loss. The retinal pigment epithelium (RPE) plays a crucial role in retinal physiology but is vulnerable to oxidative damage. We investigated the protective effects of selenium (Se) on retinal pigment epithelium (ARPE-19) and primary human retinal microvascular endothelial (ACBRI 181) cells against high glucose (HG)-induced oxidative stress and apoptotic cascade. To achieve this objective, we utilized varying concentrations of D-glucose (ranging from 5 to 80 mM) to induce the HG model. HG-induced oxidative stress in ARPE-19 and ACBRI 181 cells and the apoptotic cascade were evaluated by determining Ca2+ overload, mitochondrial membrane depolarization, caspase-3/-9 activation, intracellular reactive oxygen species (ROS), lipid peroxidation (LP), glutathione (GSH), glutathione peroxidase (GSH-Px), vascular endothelial growth factor (VEGF) and apoptosis levels. A cell viability assay utilizing MTT was conducted to ascertain the optimal concentration of Se to be employed. The quantification of MTT, ROS, VEGF levels, and caspase-3 and-9 activation was accomplished using a plate reader. To quantitatively assess LP and GSH levels, GSH-Px activities were utilized by spectrophotometer and apoptosis, mitochondrial membrane depolarization, and the release of Ca2+ from intracellular stores were evaluated by spectrofluorometer. Our investigation revealed a significant augmentation in oxidative stress induced by HG, leading to cellular damage through modulation of mitochondrial membrane potential, ROS levels, and intracellular Ca2+ release. Incubation with Se resulted in a notable reduction in ROS production induced by HG, as well as a reduction in apoptosis and the activation of caspase-3 and-9. Additionally, Se incubation led to decreased levels of VEGF and LP while concurrently increasing levels of GSH and GSH-Px. The findings from this study strongly suggest that Se exerts a protective effect on ARPE-19 and ACBRI 181 cells against HG-induced oxidative stress and apoptosis. This protective mechanism is partially mediated through the intracellular Ca2+ signaling pathway.en_US
dc.identifier.doi10.3390/molecules28165961
dc.identifier.issn1420-3049
dc.identifier.issue16en_US
dc.identifier.pmid37630213en_US
dc.identifier.pmid37630213
dc.identifier.scopus2-s2.0-85168731216
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.3390/molecules28165961
dc.identifier.urihttps://hdl.handle.net/11492/7985
dc.identifier.volume28en_US
dc.identifier.wosWOS:001056375800001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Sceince
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherMdpien_US
dc.relation.ispartofMoleculesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmzkmusnmz
dc.subjectARPE-19 cellsen_US
dc.subjecthigh glucoseen_US
dc.subjectoxidative stressen_US
dc.subjectseleniumen_US
dc.titleSelenium Protects ARPE-19 and ACBRI 181 Cells against High Glucose-Induced Oxidative Stressen_US
dc.typeArticle

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