Neuroprotective role of a protoberberine alkaloid against aluminum-induced neuroinflammation and excitotoxicity

Abstract

The study was performed to investigate the possible neuroprotective role of palmatine, a protoberberine alkaloid against aluminum-induced aberration in neurotransmitter levels, excitotoxicity, neuronal inflammation, damage, and degeneration. 100 mg/kg of aluminum chloride served as the inducing agent and was administered orally to male Wistar albino rats for 42 consecutive days. Animals were divided into four groups, groups I, II, III, and IV which involve the normal group, the toxic control group receiving aluminum chloride, and two treatment groups administered orally with palmatine at a dose of 10 mg/kg and 20 mg/kg respectively followed by aluminum chloride. Expression of neuronal inflammatory markers like IL-6 and TNF- α were checked by the ELISA method. Deranged neurotransmitter levels of acetylcholine esterase and glutamate in rat brains were measured to determine the extent of excitotoxicity. The neuroprotective role of palmatine was determined based on histopathological studies and by determining BDNF expression by the immunohistochemistry method in rat brains. Palmatine treatment effectively regulated acetylcholinesterase levels and glutamate levels otherwise elevated by aluminum. It lowered excitotoxic damage induced by aluminum and lowered the degree of expression of inflammatory markers IL-6 and TNF- α. Improved expression of BDNF in palmatine-treated groups is indicative of the neuroprotective potential of palmatine in the restoration of neuroplasticity. Histopathology further confirms the neuroprotective potential of palmatine as the treatment significantly prevented neuronal damage degeneration and loss and restored healthy and viable neurons. The findings of the study confirm the neuroprotective potential of palmatine against aluminum-induced neuroinflammation and excitotoxicity.