Mitoprotective effect of Centella asiatica against aluminum-induced neurotoxicity in rats: possible relevance to its anti-oxidant and anti-apoptosis mechanism.

Role of mitochondrial dysfunction and oxidative stress has been well documented in various cognitive-related disorders such as Alzheimer's disease. Aluminum is a neurotoxic metal that may be involved in the progression of neurodegenerative processes. The antioxidant and memory enhancing effects of Centella asiatica (CA) are well known in the last few decades. Therefore, the present study has been designed to explore the neuroprotective effect of CA on chronic aluminum exposure induced mitochondrial enzyme alteration, oxidative stress, apoptosis and cognitive dysfunction in rat. Aluminum (100 mg/kg) and CA (150 and 300 mg/kg) were administered daily for a period of 6 weeks in male Wistar rats. Various behavioral, biochemical and cellular estimations and aluminum concentration were assessed. Chronic aluminum administration resulted in memory impairment and caused marked oxidative damage associated with mitochondria impairment. It also caused a significant increase in caspase-3 activity, acetylcholine esterase activity and aluminum concentration in hippocampus and cerebral cortex of rat brain. Chronic administration of CA significantly improved memory performance, oxidative defense decreased aluminum concentration, caspase-3, acetylcholinestrease activity and reversal of mitochondrial enzyme activity as compared to aluminum-treated animals. Results of the study demonstrate neuroprotective potential of CA against aluminum-induced cognitive dysfunction and mito- oxidative damage.