ABSTRACT
Cymbopogon citratus is a tropical phytomedicinal plant that is widely known for its hypoglycemic, hypolipidemic, anxiolytic, sedative, antioxidative and anti-inflammatory properties. In this study, we have examined the neuroprotective effects of the essential oil (ESO) of Cymbopogon citratus, following aluminum chloride (AlCl3)-induced neurotoxicity within the cerebellum of Wistar rats. A total of 40 adult male Wistar rats were assigned into five groups and treated orally as follows: A–phosphate-buffered saline (1 ml daily for 15 days); B–ESO (50 mg/kg daily for 15 days); C–AlCl3 (100 mg/kg daily for 15 days); D–AlCl3 then ESO (100 mg/kg AlCl3 daily for 15 days followed by 50 mg/kg ESO daily for subsequent 15 days); E– ESO then AlCl3 (50 mg/kg ESO daily for 15 days followed by 100 mg/kg AlCl3 daily for following 15 days). To address our questions, we observed the locomotion and exploratory behavior of the rats in the open field apparatus and subsequently evaluated cerebellar oxidative redox parameters, neural bioenergetics, acetylcholinesterase levels, transferrin receptor protein, and total protein profiles by biochemical assays. Furthermore, we investigated cerebellar histomorphology and Nissl profile by H&E and Cresyl violet Nissl staining procedures. ESO treatment markedly attenuated deficits in exploratory activities and rearing behavior following AlCl3 toxicity, indicating its anxiolytic potentials. Additionally, AlCl3 evokedincrease in malondialdehyde and nitric oxide levels, as well as repressed cerebellar catalase, glutathione peroxidase, and superoxide dismutase profiles were normalised to baseline levels by ESO treatment. Treatment with ESO, ergo, exhibits substantial neuroprotective and modulatory potentials in response to AlCl3 toxicity.
ABSTRACT
Cymbopogon citratus is a tropical phytomedicinal plant that is widely known for its hypoglycemic, hypolipidemic, anxiolytic, sedative, antioxidative and anti-inflammatory properties. In this study, we have examined the neuroprotective effects of the essential oil (ESO) of Cymbopogon citratus, following aluminum chloride (AlCl3)-induced neurotoxicity within the cerebellum of Wistar rats. A total of 40 adult male Wistar rats were assigned into five groups and treated orally as follows: A–phosphate-buffered saline (1 ml daily for 15 days); B–ESO (50 mg/kg daily for 15 days); C–AlCl3 (100 mg/kg daily for 15 days); D–AlCl3 then ESO (100 mg/kg AlCl3 daily for 15 days followed by 50 mg/kg ESO daily for subsequent 15 days); E– ESO then AlCl3 (50 mg/kg ESO daily for 15 days followed by 100 mg/kg AlCl3 daily for following 15 days). To address our questions, we observed the locomotion and exploratory behavior of the rats in the open field apparatus and subsequently evaluated cerebellar oxidative redox parameters, neural bioenergetics, acetylcholinesterase levels, transferrin receptor protein, and total protein profiles by biochemical assays. Furthermore, we investigated cerebellar histomorphology and Nissl profile by H&E and Cresyl violet Nissl staining procedures. ESO treatment markedly attenuated deficits in exploratory activities and rearing behavior following AlCl3 toxicity, indicating its anxiolytic potentials. Additionally, AlCl3 evokedincrease in malondialdehyde and nitric oxide levels, as well as repressed cerebellar catalase, glutathione peroxidase, and superoxide dismutase profiles were normalised to baseline levels by ESO treatment. Treatment with ESO, ergo, exhibits substantial neuroprotective and modulatory potentials in response to AlCl3 toxicity.
ABSTRACT
Background: Nicotine is the addictive component oftobacco smoking. It has been reported to have anegative neuromodulatory role in the CNS. Moringaoleifera is a medicinal plant with reported antioxidant,anticonvulsant, anti-inflammatory and neuroprotective properties. Aim and Objectives: This studywas purposed to investigate the neuronal adaptationpotentials of Moringa Oleifera (MO) on nicotineinduced behavioural decline and perturbed bioenergetics. Material and Methods: Twenty-four adultmale Wistar rats were used. The treatment regimen wasas follows; control group received distilled water, MOgroup received 200 mg/kg of MO, Nicotine Groupreceived 1.38 mg/kg body weight of nicotine, andNicotine + MO group received combined treatment of200 mg/kg body weight of MO after 1.38 mg/kg bodyweight of nicotine for 28 days. The animals weresubjected to Morris water maze for spatial memory, Ymaze for working memory and elevated-plus mazetests for anxiety levels after which they were sacrificedfor spectrophotometric analysis of global proteinexpression, neural bioenergetics (lactate dehydrogenase and glucose-6-phosphate dehydrogenase), andAcetylcholinesterase (AChE) levels. Results: Nicotineinfusion caused a reduction in the escape latencyperiod, increased the percentage incorrect alternation,and elevated the anxiety levels of rats. Theseobservations were indicative of decreased synapticactivity in the brain. Together with, nicotine inducedchromatolytic changes in cells of the frontal cortex andhippocampus. Co-administration with MO preventednicotine-associated memory decline, perturbedglucose bioenergetics, induced chromatolysis andhistomorphological distortion in the frontal cortex andhippocampus. Conclusion: Our data demonstrate thatMO administration enhances experience-dependentneuroplasticity and cognitive behaviour function inlaboratory animals, modulates energy metabolism andreduced oxidant stress possibly through enhancedproduction of key antioxidant enzymes against thedamaging effects of nicotine. It provided evidence thatMO can be further developed as a means to protect thebrain from oxidative stress-induced injury.