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Berberine protects against behavioral deficits, memory dysfunction, and callosal demyelination in cuprizone-intoxicated C57BL/6 mice.

Created on 15 Oct 2026

Authors

Mohaddeseh Sadat Alavi, Seyede Faeze Hosseini, Amir Afkhami-Goli, Mahsa Aminizade, Emad Mokarramdust, Naghmeh Layegh Khavidaki, Fatemeh Forouzanfar, Hamid Reza Sadeghnia

Published in

Iranian journal of basic medical sciences. Volume 29. Issue 9. Pages 1398-1405.

Abstract

Multiple sclerosis (MS) is a neurological disorder marked by progressive demyelination and neuroinflammation. Berberine, a plant-derived isoquinoline alkaloid found in Berberis species, has notable anti-inflammatory and antioxidant properties. This study aimed to evaluate berberine's protective effects against cuprizone intoxication in C57BL/6 mice.
C57BL/6 mice received a cuprizone-containing diet (0.2% w/w) for five weeks and were concurrently treated with berberine (5 or 10 mg/kg). Body weight, motor coordination, exploratory and locomotor activity, memory function, oxidative stress biomarkers, and inflammatory cytokines were assessed. Histopathological evaluation of myelination was performed using Luxol Fast Blue staining.
Berberine treatment improved exploratory behavior, locomotor activity, and memory function compared with cuprizone-only mice. Oxidative stress analysis showed that berberine significantly reduced malondialdehyde (MDA) levels and increased total thiol content. Berberine also attenuated cuprizone-induced increases in interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Histological findings indicated that berberine preserved myelin integrity, prevented myelin degradation, and reduced the severity of demyelination in the corpus callosum.
These findings indicate that berberine confers protective effects against cuprizone-induced behavioral deficits, memory dysfunction, and callosal demyelination in C57BL/6 mice. The neuroprotective actions of berberine appear to be mediated by suppression of oxidative stress and inflammatory cytokines.

PMID:
42703304
Bibliographic data and abstract were imported from PubMed on 15 Oct 2026.

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