ArticleBrain sciences2025
Naringenin's Neuroprotective Effect on Diazino-Induced Cerebellar Damage in Male Albino Rats, with Modulation of Acetylcholinesterase.
Article in Brain sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Oxidative stress and antioxidant therapeutics in autism spectrum disorder: a biochemical and structure-activity relationship perspective.Molecular diversity · 2026Review
- Evaluation of Polyphenol-Rich Lemon Peel Extract Use in a Zebrafish Model of Spinal Cord Injury: Morphology, Repair-Associated Markers, and Inflammatory Profile.International journal of molecular sciences · 2026Article
- Neuroprotective effects of naringenin on nicotine-induced anxiety and depression: Involvement of monoaminergic systems, oxidative stress, and neuroinflammation on male rats.Current research in pharmacology and drug discovery · 2026Article
- Promising neuroprotective potential of naringenin against trimethyltin-induced cognitive deficits and hippocampal neurodegeneration in rats.Frontiers in neuroscience · 2025Article
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Abstract
backgroundDiazinon, a well-known organophosphorus compound, is recognized for its neurotoxic effects, primarily through the inhibition of acetylcholinesterase (AChE) and induction of oxidative stress.
aimThis study evaluates the neuroprotective effects of naringenin, a citrus flavonoid, against diazinon-induced cerebellar damage in male albino rats. MATERIALS AND
methodsTwenty-four rats were divided into four groups: control, naringenin, diazinon, and diazinon with naringenin.
resultsHistological examination revealed altered structures of Purkinje cells in the cerebellum of the diazinon group. Naringenin co-treatment significantly improved cerebellar histology and modulated oxidative stress markers by decreasing malondialdehyde (MDA) and increasing glutathione (GSH) and glutathione peroxidase (GPx) levels. Additionally, naringenin exhibited anti-inflammatory effects by decreasing nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) levels, while increasing interleukin-10 (IL-10). It also reduced apoptotic markers, including p53, Bax, caspase-9, caspase-8, and caspase-3, while increasing the anti-apoptotic marker Bcl-2. Furthermore, naringenin modulated AChE activity, leading to decreased acetylcholine levels and reduced neurotoxicity.
conclusionsThese findings suggest that naringenin's antioxidant, anti-inflammatory, and anti-apoptotic properties contribute to its neuroprotective role against diazinon-induced cerebellar damage.
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