IDEMUDIA U. OSAGIE

Exposure to neurotoxic substances like nickel chloride poses significant risks to neurological health. Vinpocetine, a synthetic derivative of the alkaloid vincamine acts as a phosphodiesterase- 1 inhibitor, modulating intracellular signaling and enhancing cerebral metabolism. It improves cerebral blood flow and supports synaptic plasticity, by increasing cyclic GMP and reducing neuroinflammation and neurodegenerative damage by reducing oxidative stress. Accordingly, this study was aimed at investigating the possible neuroprotective activity of vinpocetine on Nickel Chloride-induced neurotoxicity in adult Wistar rats. In this study, Fourty-two (42) Wistar rats was randomly divided into six (6) groups (n=7). Group A rats served as the control group to be given 1ml of distilled water. Group B rats was administered Nickel Chloride only at a dose of 5mg/kg body weight. Group C rats was administered 2.5mg/kg body weight of Vinpocetine and 5mg/kg body weight of Nickel Chloride. Group D rats was administered 5mg/Kg body weight of Vinpocetine and 5mg/kg body weight of Nickel Chloride. Group E rats was administered with 2.5mg/Kg body weight of Vinpocetine only and group F rats was administered with 5mg/Kg body weight of vinpocetine. Neurobehavioral activities were assessed 24 hours before the last administration, and at the end of the experimental period, the rats were weighed and sacrificed, and the body and brain weight changes, antioxidant enzymes activity, as well as histological assessment of the cerebrum. Results indicate that nickel chloride administration led to significant decrease on body weight, brain weight, neurobehavioral activity, and antioxidant enzymes levels, while increasing lipid peroxidation. However, pretreated rats with Vinpocetine mitigated these detrimental effects induced by nickel chloride. Vinpocetine supplementation was associated with improved body and brain weight, enhanced neurobehavioral performance, elevated antioxidant enzyme levels. This study sheds light on vinpocetine's potential as a neuroprotective agent against nickel chloride-induced neurotoxicity, suggesting its importance in preventing or mitigating neurological disorder caused by nickel chloride.