Flunarizine prevents demyelination and neurological deficits in a cuprizone-induced mouse model of multiple sclerosis.

Authors

Gopika Venu, S S Binil Raj

Published in

Indian journal of pharmacology. Volume 58. Issue 5. Pages 581-590. Sep 01, 2026. Epub Sep 02, 2026.

Abstract

Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system, where demyelination occurs alongside axonal and neuronal degeneration. Current treatments focus primarily on immunomodulation and symptom management, with limited efficacy in halting or reversing demyelination. Finding drugs to treat progression of the disease remains the greatest unmet need for people with MS.
Demyelination is induced in Swiss albino mice by administering cuprizone (CPZ) 0.3% in the diet for 6 weeks. Two different doses (1.2 and 2.4 mg/kg) of flunarizine dihydrochloride were administered orally along with CPZ for a duration of six weeks. We used the rotarod apparatus and actophotometer to assess motor and locomotor activity, elevated plus maze to evaluate anxiety, and shuttle box apparatus to evaluate memory. Various biochemical parameters were estimated from brain homogenate, and the histological changes were evaluated using H and E and Luxol Fast Blue stain. The experimental data obtained were analysed by ANOVA followed by the Tukey multiple comparison test.
The result of behavioural assays showed better motor coordination, locomotion, memory, and reduced anxiety levels in the drug-treated mice. Besides, the elevated level of serotonin and the reduced levels of glutamate and catalase level in the brain homogenate of treated mice indicate its neuroprotective potential. Healthy histology appearance and increased level of myelin in the brain also substantiate the protective effect of Flunarizine.
Our experimental data suggest that flunarizine dihydrochloride attenuated the demyelination in the brain and also produced functional and behavioural improvement in demyelinated mice, suggesting its potential to manage demyelinating disorders.

PMID:
42683990
Bibliographic data and abstract were imported from PubMed on 02 Sep 2026.

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