Ameliorative Effect of Prosopis africana Seed Extract on Cobalt Chloride Induced Cerebellar Toxicity: Neurobehavioural, Histomorphological and Biochemical Findings

Abstract

Cobalt toxicity from industrial exposure and medical metal prosthesis has been linked to neurological problems such as motor dysfunction. The goal of this study was to find out whether Prosopis africana (PA) seed extract had ameliorative effects on the cerebellum of adult Wistar rats exposed to cobalt chloride (CoCl2). 60 male Wistar rats were grouped into 4 (n=15). Rats were treated with CoCl2 or CoCl2 in combination with PA seed extract (PAE) at 50mg or 100mg orally for 14 days. Control rats received distilled water for the same period. The findings showed that CoCl2 caused neurobehavioural impairment in rats by reducing exploratory activities, increasing anxiety, and significantly (p<0.05) reducing hanging latency along with a low limb impairment score. Co-treatment with PAE on the other hand, enhanced these parameters to levels comparable to control, reduced hydrogen peroxide (H2O2) and malondialdehyde (MDA) in cerebellar tissues, while also improving superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Furthermore, PAE50mg or 100mg significantly (p<0.05) reduced proinflammatory biomarkers such as Interleukin 1 beta (IL-1β) and tumour necrosis factor (TNF-α). In the histology and immunohistochemistry, CoCl2 treated groups showed severe cytoplasmic vacuolations and nuclei fragmentation in Purkinje neurons, as well as elevated astrocytic expression of glial fibrillary acidic protein (GFAP), which was alleviated by PAE therapy. Thus, when PAE was administered, cerebellar Purkinje cell integrity was improved, antioxidant status was boosted, and lipid peroxidation in the cerebellum was suppressed. Hence, PAE ameliorated CoCl2 induced alterations by reducing oxidative stress, enhancing anti-oxidant enzyme status and decreasing inflammation.