The effects of aqueous extract of ocimum gratissimum on the cerebellum of male wistar rats challenged by lead acetate

Abstract

•Chronic lead acetate toxicity was induced in male rats by oral administration.•Effect of Ocimum gratissimum in lead acetate toxicity on the cerebellum.•Oral lead acetate administration led to oxidative stress in the cerebellum.•Ocimum gratissimum extract attenuated oxidative stress and enhanced antioxidant enzymes.•Ocimum gratissimum ameliorated lead acetate-induced toxicity in the cerebellum. ObjectivesLead acetate (LA) is a known toxicant, and its exposure in the environment has been on the increase in recent times, leading to oxidative stress and tissue damage. Based on this background, we investigated the role of the antioxidative properties of Ocimum gratissimum (OG), a potent medicinal plant, in ameliorating and protecting the brain from lead acetate-induced cerebellar damage via the assessment of oxidative stress parameters and brain histology.MethodsThirty-five adult male Wistar rats weighing 145–200g divided into five groups were used for this experimental study. Groups 1, 2, and 3 served as positive and negative controls and were administered sterile water, 252.98 mg/kg body weight of aqueous leaves extract of OG and 120 mg/kg of LA for 21 days. Furthermore, following the administration of LA, rats in groups 4 and 5 were treated with 125 and 250 mg/kg body weight of OG. OG and LA were administered orally for 42 days. Oxidative stress parameters, as well as histoarchitectural investigations following LA and OG treatment, were analysed.ResultsResults showed normal histoarchitecture of the cerebellum in control and group 2 animals (OG only). In group 3 animals that received LA only, we observed severe stages of neurodegenerative features in the Purkinje, granular cell molecular cell layers of the Cerebellum. Also, results from groups 4 and 5 rats that were co-administered with LA and OG revealed regenerative tendencies and an increase in the neuronal cell density of the cerebellum. Nevertheless, we recorded an increase in the brain content of malondialdehyde and decreased antioxidant status (catalase (CAT), glutathione (GSH), and sodium dismutase (SOD)) following LA administration. OG attenuated this heightened MDA activity and depletion of the antioxidant status.ConclusionOverall, these findings suggest that oral administration of aqueous extract of OG improved cerebellar neurotoxicity and degeneration in rats exposed to LA by modulating oxidative damage. Lead acetate (LA) is a known toxicant, and its exposure in the environment has been on the increase in recent times, leading to oxidative stress and tissue damage. Based on this background, we investigated the role of the antioxidative properties of Ocimum gratissimum (OG), a potent medicinal plant, in ameliorating and protecting the brain from lead acetate-induced cerebellar damage via the assessment of oxidative stress parameters and brain histology. Thirty-five adult male Wistar rats weighing 145–200g divided into five groups were used for this experimental study. Groups 1, 2, and 3 served as positive and negative controls and were administered sterile water, 252.98 mg/kg body weight of aqueous leaves extract of OG and 120 mg/kg of LA for 21 days. Furthermore, following the administration of LA, rats in groups 4 and 5 were treated with 125 and 250 mg/kg body weight of OG. OG and LA were administered orally for 42 days. Oxidative stress parameters, as well as histoarchitectural investigations following LA and OG treatment, were analysed. Results showed normal histoarchitecture of the cerebellum in control and group 2 animals (OG only). In group 3 animals that received LA only, we observed severe stages of neurodegenerative features in the Purkinje, granular cell molecular cell layers of the Cerebellum. Also, results from groups 4 and 5 rats that were co-administered with LA and OG revealed regenerative tendencies and an increase in the neuronal cell density of the cerebellum. Nevertheless, we recorded an increase in the brain content of malondialdehyde and decreased antioxidant status (catalase (CAT), glutathione (GSH), and sodium dismutase (SOD)) following LA administration. OG attenuated this heightened MDA activity and depletion of the antioxidant status. Overall, these findings suggest that oral administration of aqueous extract of OG improved cerebellar neurotoxicity and degeneration in rats exposed to LA by modulating oxidative damage.