Protective effect of Celastrus paniculatus on cognitive function in glutamate-induced brain-injured mice by reducing the intracellular influx of Ca.

Abstract

Present investigation evaluates the protective effect of Celastrus paniculatus (CP) on the cognitive function in neuronal injured mice. Neuronal injury was induced by oral administration of monosodium glutamate (MSG) at a dose of 1.66 g/kg/day for 30 days. Mice in the CP-treated group receives CP 30 mg/kg ip and CP + GGA-treated group received CP 30 mg/kg ip and glutamic acid (GGA, 1.5mg/kg, ip) 30 min prior to the administration of MSG for 30 days. Assessment of cognitive function was done using Morris water maze. Level of inflammatory cytokines and production of reactive oxygen species (ROS) was estimated in the brain tissue of brain-injured mice. Moreover, intracellular concentration of Ca+ ion was estimated in the brain tissue and expression of Bcl-2, Bax, and caspase-3 protein was estimated in the brain tissue by western blot assay. Cognitive function was attenuated in CP-treated glutamate-injured mice. Data of the study suggest that treatment with CP reduces the level of inflammatory cytokines and production of ROS in the brain tissue compared to negative control group. There was reduction in the concentration of Ca+ ion in the neuronal cells in CP-treated group than negative control group of mice. Treatment with CP ameliorates the expression of Bax, Bcl-2, and caspase-3 in the brain tissue of glutamate-induced brain-injured mice. In conclusion, data of the study suggest that treatment with CP attenuates the cognitive function and neuronal apoptosis in glutamate-induced neuronal injury by reducing the concentration of intracellular Ca+ ion.