International ophthalmology · 2025
Assessment of neuroprotective efficacy of N-acetylcysteine compared with brimonidine in an experimental glaucoma model.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод в очереди
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Yavuz Mustafa, Acer Semra, Celik Omer, Argun Mehmet, Ozmen Ozlem, Tok Levent
Аннотация
PURPOSE: To investigate the neuroprotective effects of N-acetylcysteine (NAC) in comparison with brimonidine in an experimental glaucoma model.
METHODS: Thirty-two adult female Wistar albino rats were randomly assigned to five groups: Control, Sham, NAC, Brimonidine, and Combination (NAC + Brimonidine). Glaucoma was induced in the right eye by optic nerve crush in all groups except Control. Treatments were administered intraperitoneally every 72 h for 30 days. Neuroprotection was assessed histopathologically by measuring ganglion cell layer (GCL) thickness and total retinal thickness. Apoptotic activity and glial activation were evaluated by quantifying B-cell lymphoma/leukemia-2 (BCL-2), BCL-2-associated X protein (BAX) and glial fibrillary acidic protein (GFAP) expression. Oxidative stress and antioxidant capacity were assessed using malondialdehyde (MDA), total oxidant status (TOS), glutathione (GSH) and total antioxidant capacity (TAC) levels.
RESULTS: NAC significantly preserved GCL and total retinal thickness compared with the Sham group (P < 0.001), with neuroprotective efficacy comparable to brimonidine (P > 0.05). The combination therapy group demonstrated the most pronounced neuroprotective effects. NAC treatment increased antiapoptotic BCL-2 and GSH levels while reducing BAX, GFAP, MDA, and TOS levels (P < 0.001).
CONCLUSIONS: NAC exhibited substantial neuroprotective effects in an intraocular pressure-independent glaucoma model, likely mediated through its antioxidant properties and modulation of apoptotic pathways. These findings suggest that NAC may serve as a promising adjunctive therapy for glaucomatous optic neuropathy and other retinal neurodegenerative disorders characterized by oxidative stress and apoptosis.
METHODS: Thirty-two adult female Wistar albino rats were randomly assigned to five groups: Control, Sham, NAC, Brimonidine, and Combination (NAC + Brimonidine). Glaucoma was induced in the right eye by optic nerve crush in all groups except Control. Treatments were administered intraperitoneally every 72 h for 30 days. Neuroprotection was assessed histopathologically by measuring ganglion cell layer (GCL) thickness and total retinal thickness. Apoptotic activity and glial activation were evaluated by quantifying B-cell lymphoma/leukemia-2 (BCL-2), BCL-2-associated X protein (BAX) and glial fibrillary acidic protein (GFAP) expression. Oxidative stress and antioxidant capacity were assessed using malondialdehyde (MDA), total oxidant status (TOS), glutathione (GSH) and total antioxidant capacity (TAC) levels.
RESULTS: NAC significantly preserved GCL and total retinal thickness compared with the Sham group (P < 0.001), with neuroprotective efficacy comparable to brimonidine (P > 0.05). The combination therapy group demonstrated the most pronounced neuroprotective effects. NAC treatment increased antiapoptotic BCL-2 and GSH levels while reducing BAX, GFAP, MDA, and TOS levels (P < 0.001).
CONCLUSIONS: NAC exhibited substantial neuroprotective effects in an intraocular pressure-independent glaucoma model, likely mediated through its antioxidant properties and modulation of apoptotic pathways. These findings suggest that NAC may serve as a promising adjunctive therapy for glaucomatous optic neuropathy and other retinal neurodegenerative disorders characterized by oxidative stress and apoptosis.