ArticleAIMS neuroscience2022
Naringin ameliorates motor dysfunction and exerts neuroprotective role against vanadium-induced neurotoxicity.
Article in AIMS neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Modelling Olfactory Dysfunction in Rodents Through Intranasal Vanadium Exposure.Animals : an open access journal from MDPI · 2026Review
- Copper and vanadium induce oxidative stress and pyroptosis in the duck brain via activating the TLR4/NF-κB-p65 signaling pathway.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Article
- Exploring the neuroprotective potential of naringin following spinal cord injury in rats: improving sensory and motor function through combating inflammation and oxidative stress.Frontiers in pharmacology · 2025Article
- Characterization of an olfactory system dysfunction model: a vanadium dose-effect study via nose-to-brain delivery in rats.Frontiers in neuroanatomy · 2025Article
- Flavonoid glycoside fraction ofAIMS neuroscience · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to vanadium has been known to lead to a progressive neurodegenerative disorder like Parkinson's disease. Naringin is a known flavonoid glycoside that is mostly seen in the flesh of grapefruit and orange and is believed to have protective effects for the treatment of neurodegenerative disorders. This study sought to investigate the role of Naringin in the treatment of vanadium-induced neurotoxicity. Vanadium (10 mg/kg BW) was injected intraperitoneally to induce motor dysfunction, followed by treatment with Naringin (30 mg/kg BW) intraperitoneally for 14 days. Oxidative stress imbalance was monitored by checking Glutathione Peroxidase (GPX) and Catalase levels. Histological and immunohistochemical alterations were observed using RBFOX3 polyclonal antibody to determine neuronal cell distribution and NLRP3 inflammasome antibody as a marker of inflammation. Exposure to vanadium induces neurotoxicity by significantly increasing the Catalase and Glutathione Peroxidase (GPX) levels. Vanadium administration also led to increased inflammatory cells and a significant reduction of the viable neuronal cells in the SNc and CPu. Treatment with Naringin showed a neuroprotective role by dependently restoring the Catalase and Glutathione Peroxidase (GPX) levels, inflammasome activation, and neuronal damage in the SNc and CPu. Naringin demonstrated anti-oxidative, and anti-inflammatory responses by inhibiting oxidative stress, and inflammation and exerts neuroprotective effects by inhibiting apoptosis following vanadium-induced neurotoxicity in adult Wistar rats.
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