Abstract

Nicotine present in the tobacco leaves are activated through nicotinic acetylcholine receptors and are involved in neurobehavioral activity. Despite creating awareness, there is an increasing trend in the consumption of tobacco. Few plant products have been documented to protect the pathological consequences of nicotine. The present study is aimed to find the beneficial effects of Bacopa-Monnieri (BM) against nicotine induced physical, psychological, neurobehavioral and biochemical changes in cerebellum. Thirty-two male Sprague-Dawley rats (220-235g) were equally randomized into four groups: Group I: Control; received normal Saline. Group II: received Nicotine (5mg/kg Body-Weight) for 90 days. Group III: received nicotine (5mg/ kg Body-Weight) for initial 90 days followed by Bacopa-Monnieri (100mg/kg Body-Weight) for next 90 days. Group IV: received Bacopa-Monnieri (100 mg/kg Body-Weight) for 90 days. All compounds were administered through oral gavage. Rats were subjected to Open Field Test, Elevated Plus Maze and Beam Walking Test. Following behavioral tests, rats were anesthetized with ketamine (80 ml/kg Body-Weight) and xylocaine (100 ml/kg Body-Weight), brain was dissected and cerebellum was separated. Concentration of Malondialdehyde, Nitric Oxide and activity of Glutathione Peroxidase were measured spectrophotometrically in the supernatant of cerebellum tissue homogenates. Nicotine increases the Malondialdehyde (MDA) and Nitric-Oxide (NO) level in cerebellar tissue compared to control. Nicotine induced increase in Malondialdehyde and Nitric-Oxide level were prevented by Bacopa-Monnieri. The Glutathione Peroxidase (GPx) activity was lower in nicotine treated rats whereas oral supplementation of Bacopa-Monnieri significantly increases the activity of Gluathione-Peroxidase. Bacopa-Monnieri supplementations significantly reverse the Nicotine induced reduction in locomotion activity, exploratory behavior, anxiety, motor impairment and balance. Bacopa-Monnieri confers the protective effects against nicotine induced neurobehavioral alteration and oxidative stress in rats.

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