DOI: 10.11648/j.cnn.20261002.12 ISSN: 2578-8930

Kolaviron and Bryophyllum pinnatum Attenuate AlCl 3 -Induced Memory Impairment by Modulating Oxidative Stress, Astrogliosis, and Bcl-2/Nrf2 Signaling

Rademene Oria, Bolaji Mesole, Ujong Otu, Kingsley Akpang, Saviour Usin, Cynthia Tangban, Sesugh Ugese, Comfort Ugbong, Chidera Nwodo, Oluchi Uwazurike, Chinecherem Obidinanwa, Margaret Michael
Background: Chronic exposure to aluminium chloride (AlCl 3 ) damages the hippocampus and impairs cognition through oxidative stress, reactive astrogliosis, and neuronal apoptosis. Phytochemicals with antioxidant and anti-inflammatory activity are increasingly considered as candidate neuroprotectants, yet evidence supporting combined plant-derived interventions that target these convergent pathways remains scarce. Purpose: This study examined whether Kolaviron, a biflavonoid complex from Garcinia kola seeds, and an ethanolic extract of Bryophyllum pinnatum (CRA), administered individually or in combination, attenuate AlCl 3 -induced hippocampal injury and cognitive impairment in Wistar rats, and whether their protective actions converge on the Nrf2 signalling pathway. Methods: Seventy adult male Wistar rats were randomly assigned to seven groups of ten: vehicle control, AlCl 3 (100 mg/kg), Kolaviron alone (200 mg/kg), CRA alone (600 mg/kg), AlCl 3 + Kolaviron, AlCl 3 + CRA, and AlCl 3 + Kolaviron + CRA. All agents were administered by oral gavage daily for fourteen days. Spatial learning and memory were assessed using the Morris water maze. Hippocampal homogenates were assayed for superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA). Haematoxylin and eosin staining was used to evaluate cytoarchitecture, and immunohistochemistry quantified glial fibrillary acidic protein (GFAP), B-cell lymphoma 2 (Bcl-2), and nuclear factor erythroid 2-related factor 2 (Nrf2) expression in the CA3 subfield. Data were analysed by one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. Results: AlCl 3 exposure prolonged escape latency, lowered SOD and CAT activities, raised MDA, produced neuronal loss with pyknotic and vacuolated cells, increased GFAP immunoreactivity, and reduced both Bcl-2 and Nrf2 expression in CA3. Co-treatment with Kolaviron or CRA reversed each of these alterations (p < 0.05 versus AlCl 3 alone), and the combined regimen produced the most consistent restoration across behavioural, biochemical, histological, and immunohistochemical endpoints, frequently returning values close to control levels. Conclusion: Kolaviron and B. pinnatum protect the rat hippocampus against AlCl 3 -induced damage by restoring antioxidant defences, attenuating astrogliosis, preserving Bcl-2 expression, and activating Nrf2 signalling, with the combination conferring broader protection than either agent alone. These findings support further investigation of these phytochemicals as candidates against environmental neurotoxicant-induced neurodegeneration.

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