Potential role of some nutraceuticals in neurotoxicity induced by aluminum oxide in experimental animal model

The present study aimed to evaluate neurorestorative potential of lecithin (L) and/or gallic acid (GA) in alleviating aluminum (Al)-induced neurotoxicity in rat brain. Rats were classified into seven groups: Group (1): served as control, Groups (2)&(3): received lecithin or gallic acid in a dose of 100 mg/kg body weight. Group (4): received Al in a dose of 300 mg/kg body weight, Group (5): received Al + lecithin, Group (6): received Al + gallic acid and Group (7): received Al + lecithin+ gallic acid. Rats treated orally for 28 days (5days/week). Al induced a significant increase in AChE activity, along with a significant decrease in dopamine (DA), norepinephrine (NE) and serotonin (5-HT) levels. Al treatment resulted in significant increase in malondialdehyde (MDA), nitric oxide (NO) and oxidized glutathione (GSSG) content. On the contrary, Al caused a significant decrease in glutathione (GSH) and GSH/GSSG ratio. As well as, it stimulates an apoptotic signaling program by increase of Bax, caspase-3 and Bax/Bcl-2 ratio accompanied with decrease of Bcl-2 in the tested brain areas. Histopathological examination confirms the biochemical results. Conclusively, treatment with lecithin and/or gallic acid can retrieve the effect of aluminum toxicities on the basis of cholinergic, dopaminergic, oxidative, and apoptotic status.