Abstract

Aluminium (Al) is a widely existing neurotoxic metal in the environment. Al exposure will alter several ions in the body and causes toxicity to the body by several means. Such as apoptosis, oxidative stress, disruption in neuronal transport, mitochondrial damage, excitotoxicity, generation of inflammatory mediators, and microglial activation. These mechanisms lead to several neurodegenerative diseases including sALS. The multifaceted pathogenesis makes the sALS challengeable to find a suitable treatment for the disease development and progression. In this study, we have studied the neuroprotective effects of WL and GA in the pathogenesis of sALS by using AlCl3-induced neurotoxicity model. The study was conducted on male Wistar rats. The effects of wedelolactone and gallic acid on motor learning ability, motor coordination, locomotor activity, cytokine production, glutathione peroxidase (GPx), m-calpain, caspase-3 inhibition and L-glutamate level were assessed. The reports suggest that WL and GA were dose-dependently effective in managing the toxicity caused by the exposure of AlCl3. Both (WL & GA) could able to reverse the AlCl3-induced neurotoxicity and can improve the motor learning ability, locomotor activity in the rats. Histopathological results of the cerebellum, hippocampus, striatum, and spinal cord of the rats further confirms the neuroprotective effects of WL and GA.