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Schizophrenia and related psychiatric disorders are often characterized by hippocampal dysfunction and  demyelination. Cuprizone (CPZ), a copper chelator, is commonly used to induce neurotoxicity and oxidative stress  in rodent models to mimic these dysfunctions. This study investigated the neuroprotective potential of Kolaviron  (Kv), a biflavonoid complex from Garcinia kola, against CPZ-induced hippocampal damage. Twenty-eight male  Wistar rats were divided into four groups: Control (corn oil), CPZ (0.2% diet), Kv (200 mg/kg), and Kv+CPZ.  Following 42 days of treatment, hippocampal health was assessed through biochemical assays for oxidative stress  (SOD, GPx, and MDA), and histological evaluation using H&E, Cresyl Fast Violet (Nissl profiling), and GFAP  immunohistochemistry. The results show that CPZ administration significantly decreased antioxidant enzyme  activities (SOD and GPx) and increased lipid peroxidation (MDA levels) in the hippocampus. Pyknotic changes  and disorganized pyramidal neurons were evident in the CA1-CA3 regions, and significant chromatolysis.  Furthermore, increased GFAP-positive reactive astrocytes were seen as a result of astrogliosis induced by CPZ.  Conversely, concurrent administration of Kolaviron significantly mitigated these effects, restoring antioxidant  levels, reducing MDA, and preserving the morphological integrity of pyramidal neurons and astrocytes. In  conclusion, Kolaviron exhibits significant neuroprotective properties against cuprizone-induced hippocampal  impairment. Its ability to suppress oxidative stress, maintain Nissl substance, and prevent reactive astrogliosis  suggests that Kolaviron may be a viable therapeutic candidate for managing neurodegenerative and psychiatric  disorders associated with hippocampal oxidative damage. 

Key Words: kolaviron, cuprizone, hippocampus, oxidative stress, neuroprotection