Activity of Vinpocetine in the Cerebellum of Nickel Chloride-Exposed Rats: An in-vivo and in-silico Study
DOI:
https://doi.org/10.26538/tjdr/v2i5.4Keywords:
Nickel Chloride, Vinpocetine, Cerebellum, Caspase-3, NF-κBAbstract
Purpose: Nickel chloride (NiCl2), widely used in industry, poses neurotoxic risks, particularly to the cerebellum, which regulates motor and cognitive functions. Vinpocetine, an antioxidant and anti-inflammatory agent, may offer neuroprotection. This study investigated vinpocetine’s protective effects against NiCl2-induced cerebellar toxicity in Wistar rats.
Methods: Forty-eight (42) Wistar rats were randomly distributed to six groups (n=8) and received the following treatments. Group A (control) - 1 ml distilled water; Group B - 5 mg/kg NiCl2; Groups C and D - 2.5 mg/kg and 5 mg/kg vinpocetine, respectively, alongside 5 mg/kg NiCl2; Groups E and F - 2.5 mg/kg and 5 mg/kg vinpocetine, respectively. Treatments were administered orally for 28 days, followed by neurobehavioral, oxidative stress, histological, and in-silico assessments.
Results: NiCl2 significantly (p<0.05) reduced body, brain, and relative cerebellar weight. Behavioral deficits included impaired grip strength, coordination, and mobility. Oxidative stress markers showed reduced antioxidant enzymes activity and elevated lipid peroxidation. Histological examination revealed Purkinje cell degeneration and pyknotic nuclei in NiCl2-exposed rats. Vinpocetine treatment significantly improved motor function, antioxidant activity, and cerebellar structure while reducing oxidative damage.
Conclusion: These findings suggest that vinpocetine protects against NiCl2-induced cerebellar toxicity in Wistar rats
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