Can metformin modulate the retinal degenerative changes in a rat model of retinitis pigmentosa?

Retinitis pigmentosa (RP) affects over a million people worldwide, characterized by photoreceptor cell death, progressive retinal degeneration, and visual loss. Metformin is demonstrated as a potential therapeutic approach for preventing light-induced retinal degeneration by decreasing apoptosis and...

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Veröffentlicht in:Tissue & cell 2022-06, Vol.76, p.101786-101786, Article 101786
Hauptverfasser: Eltony, Sohair A., Mohaseb, Heba S., Ahmed, Amel A., Sayed, Manal M.
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Ahmed, Amel A.
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description Retinitis pigmentosa (RP) affects over a million people worldwide, characterized by photoreceptor cell death, progressive retinal degeneration, and visual loss. Metformin is demonstrated as a potential therapeutic approach for preventing light-induced retinal degeneration by decreasing apoptosis and oxidative stress. This work aimed to investigate the effect of metformin on the retina of the N-Ethyl-N-nitrosourea (ENU) induced rat model of RP. Eighteen adult male Wistar rats were divided into two groups. Group I: normal vehicle control (N = 6). Group II: ENU-induced photoreceptor degeneration (N = 12) received a single intraperitoneal injection of ENU at a 600 mg/kg dose. Rats in group II were equally divided into two subgroups: IIa: photoreceptor degeneration-induced group and IIb: metformin-treated group (200 mg/kg) for seven days. Specimens from the retina were processed for light and electron microscopy. In ENU treated group, the retina revealed vacuolations and morphological changes in the glia (Müller cells and microglia) and blood capillaries. Increasing caspase-3 (apoptotic marker), iNOS (oxidative stress marker), CD68 (macrophage marker) and glial fibrillary acidic protein (GFAP) expression were detected. In the metformin-treated group, the retinal vacuolations reduced with the morphological improvement in the glia and blood capillaries. Caspase-3, iNOS, CD68, and GFAP expression decreased. Metformin was found to have a neuroprotective effect on the retina in ENU induced rat model of RP •Retinitis pigmentosa (RP) is a cause of inherited blindness characterized by photoreceptor cell death.•Metformin is demonstrated to prevent light-induced retinal degeneration by decreasing apoptosis and oxidative stress.•This study investigated the effect of metformin on the retina of N-Ethyl-N-nitrosourea (ENU) induced rat model of RP.•Metformin suppressed microglia and Müller cells activation and improved the changes in the retinal blood capillaries.•Metformin was found to have a neuroprotective effect on the retina in ENU induced rat model of RP.
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Increasing caspase-3 (apoptotic marker), iNOS (oxidative stress marker), CD68 (macrophage marker) and glial fibrillary acidic protein (GFAP) expression were detected. In the metformin-treated group, the retinal vacuolations reduced with the morphological improvement in the glia and blood capillaries. Caspase-3, iNOS, CD68, and GFAP expression decreased. 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Metformin is demonstrated as a potential therapeutic approach for preventing light-induced retinal degeneration by decreasing apoptosis and oxidative stress. This work aimed to investigate the effect of metformin on the retina of the N-Ethyl-N-nitrosourea (ENU) induced rat model of RP. Eighteen adult male Wistar rats were divided into two groups. Group I: normal vehicle control (N = 6). Group II: ENU-induced photoreceptor degeneration (N = 12) received a single intraperitoneal injection of ENU at a 600 mg/kg dose. Rats in group II were equally divided into two subgroups: IIa: photoreceptor degeneration-induced group and IIb: metformin-treated group (200 mg/kg) for seven days. Specimens from the retina were processed for light and electron microscopy. In ENU treated group, the retina revealed vacuolations and morphological changes in the glia (Müller cells and microglia) and blood capillaries. Increasing caspase-3 (apoptotic marker), iNOS (oxidative stress marker), CD68 (macrophage marker) and glial fibrillary acidic protein (GFAP) expression were detected. In the metformin-treated group, the retinal vacuolations reduced with the morphological improvement in the glia and blood capillaries. Caspase-3, iNOS, CD68, and GFAP expression decreased. Metformin was found to have a neuroprotective effect on the retina in ENU induced rat model of RP •Retinitis pigmentosa (RP) is a cause of inherited blindness characterized by photoreceptor cell death.•Metformin is demonstrated to prevent light-induced retinal degeneration by decreasing apoptosis and oxidative stress.•This study investigated the effect of metformin on the retina of N-Ethyl-N-nitrosourea (ENU) induced rat model of RP.•Metformin suppressed microglia and Müller cells activation and improved the changes in the retinal blood capillaries.•Metformin was found to have a neuroprotective effect on the retina in ENU induced rat model of RP.</abstract><cop>Scotland</cop><pub>Elsevier Ltd</pub><pmid>35325673</pmid><doi>10.1016/j.tice.2022.101786</doi><tpages>1</tpages></addata></record>
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source Elsevier ScienceDirect Journals
subjects Acidic oxides
Animal models
Apoptosis
Blood
Blood vessels
Capillaries
Caspase-3
Cell death
Degeneration
Electron microscopy
Ethyl nitrosourea
Glial fibrillary acidic protein
Macrophages
Markers
Metformin
Microglia
Morphology
Mueller cells
Neuroprotection
Nitric-oxide synthase
Oxidative stress
Photoreceptor degeneration
Photoreceptors
Retina
Retinal degeneration
Retinitis
Retinitis pigmentosa
Rodents
Subgroups
title Can metformin modulate the retinal degenerative changes in a rat model of retinitis pigmentosa?
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