Asiatic acid nullified aluminium toxicity in in vitro model of Alzheimer's disease.

Aluminium (Al) is a ubiquitously distributed environmental toxicant that lacks biological functions; however, its accumulation in the brain has been demonstrated to be linked to several neuropathological conditions particularly Alzheimer's disease (AD). Asiatic acid (AA), a triterpene extracted from Centella asiatica, has been reported to cross the blood brain barrier and also displayed antioxidant and neuroprotective activities. The present study was aimed to explore the neuroprotective effect of AA against aluminium maltolate (Al(mal)3) induced neurotoxicity by assessing cell viability, mitochondrial membrane potential, levels of reactive oxygen species (ROS), DNA damage and apoptosis (Hoechst and dual staining, comet assay; expressions of pro-apoptotic, anti-apoptotic and signaling indices) via AKT/GSK-3β signaling pathway in SH-SY 5Y  neuroblastoma cells. Pre-treatment with AA significantly enhanced cell viability, attenuated rotenone-induced ROS, mitochondrial membrane dysfunction and apoptosis regulating AKT/GSK-3β signaling pathway. Downregulation of Al induced neurodegeneration may be one of the approaches to control the impairment of metal ion homeostasis leading to neuronal injury in  early development of AD. However, more extensive work in animal model is desirable to confirm its neuroprotective action.