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Updated: Sep 8, 2026

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
Published on: September 21, 2021
Berberine protects against behavioral deficits, memory dysfunction, and callosal demyelination in
Mohaddeseh Sadat Alavi1,2, Seyede Faeze Hosseini3, Amir Afkhami-Goli3
1Pharmacological Research Center of Medicinal Plants, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Objectives:
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.
Materials And Methods:
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.
Results:
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.
Conclusion:
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.
