Glaucoma causes redox imbalance in the primary visual cortex by modulating NADPH oxidase-4, iNOS, and Nrf2 pathway in a rat experimental model
Abstract
The aim of this study was to elucidate the intracellular sources of oxidant species, the antioxidant response as well as the main signaling pathways involved in the regulation of the redox balance in the primary visual cortex of rats subjected to an experimental glaucoma model. 3-month female Wistar strain rats were operated under a microscope by cauterizing two of the episcleral veins in order to elevate the intraocular pressure (glaucoma group); the control group received a sham procedure. Seven days after surgery, the animals were sacrificed, the brains were carefully removed, and the primary visual cortex was dissected. NADPH oxidase (NOX) activity, as well as the inducible nitric oxide synthase (iNOS) expression, the enzymatic antioxidant defenses, the metabolism of glutathione, and the translocation of Nuclear factor-erythroid 2-related factor-2 (Nrf2) and Nuclear factor k-light-chain-enhancer of activated B cells (NF-κB) were assessed. Compared to control, glaucoma group displayed an increase in NOX activity (147%, p < 0.05), leading to a rise in the steady state concentration of oxidant species. Specifically, NOX4 expression was higher (90%, p < 0.05), suggesting that it could be a source of H2O2. In addition, iNOS expression was increased in glaucoma (47%, p < 0.05), as a source of NO in the brain, induced by NF-κB translocation to the nucleus (48%, p < 0.01). An increase in primary antioxidant enzymes superoxide dismutase (40%, p < 0.01) and glutathione peroxidase…
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