Rademene Oria - Department of Human Anatomy, Faculty of Basic Medical Sciences, Cross River University of Technology (CRUTECH), Okuku Campus, Cross River, Nigeria
Runyi Ben - Department of Human Anatomy, Faculty of Basic Medical Sciences, Cross River University of Technology (CRUTECH), Okuku Campus, Cross River, Nigeria
Ugochukwu Esomonu - Department of Human Anatomy, Faculty of Basic Medical Sciences, Cross River University of Technology (CRUTECH), Okuku Campus, Cross River, Nigeria
Precious Essien - Department of Human Anatomy, Faculty of Basic Medical Sciences, Cross River University of Technology (CRUTECH), Okuku Campus, Cross River, Nigeria
Linda Odinaka - Department of Human Anatomy, Faculty of Basic Medical Sciences, Cross River University of Technology (CRUTECH), Okuku Campus, Cross River, Nigeria
Gift Etta - Department of Human Anatomy, Faculty of Basic Medical Sciences, Cross River University of Technology (CRUTECH), Okuku Campus, Cross River, Nigeria
Otu Eyong - Department of Human Anatomy, Faculty of Basic Medical Sciences, Cross River University of Technology (CRUTECH), Okuku Campus, Cross River, Nigeria
Omamuyovwi Ijomone - The Neuro- Lab, School of Basic Medical Sciences, Federal University of Technology, Akure, Nigeria

Objective(s): Cobalt toxicity has become a health concern in recent years, due to overexposure resulting in neurological impairments. With a growing interest in the therapeutic roles of herbs, in toxicity research, it’s worth looking into the curative effects of aqueous Prosopis africana seed extract, a plant rich in flavonoids on cobalt-induced neurotoxicity. Materials and Methods: We treated rats with CoCl۲ or CoCl۲ in combination with aqueous PA seed extract (PAE) orally for ۱۴ days. Control rats received distilled water for the same period. Following treatments, behavioral experiments, analysis for oxidative stress, inflammation, and histological and immunohistochemical analysis were performed. Results: Results revealed that CoCl۲ reduced the exploration time, recognition index in the novel object recognition test, percentage spontaneous alternation in the Y-maze tests, and reduced open arm entry and duration in elevated plus-maze. However, treatment with PAE improved these parameters to levels comparable with those of the control group. Furthermore, PAE therapy reduced CoCl۲-induced surge in hydrogen peroxide, malondialdehyde, TNF-α and IL-۱β levels in brain homogenate, while also increasing superoxide dismutase and reduced reduced-glutathione activities. CoCl۲ exposure resulted in obvious features of neurodegeneration like nuclear disintegration, nuclear shrinkage, and cytoplasmic vacuolations of the cells of the hippocampus and amygdala, with an increased expression of GFAP. The hippocampal and amygdala histology improved after PAE administration, while exacerbated GFAP expressions were attenuated. Conclusion: These findings imply that PAE may be anxiolytic and can help reduce cognitive impairments and hippocampal damage caused by CoCl۲ neurotoxicity, via mechanisms that involve attenuation of oxidative stress and inflammation.

Amygdala, Cobalt, Hippocampus, Neuroinflammation, Neurotoxicity, Oxidative stress, Prosopis africana