Ethanol-Soluble Extract of Terminalia chebula Attenuates Paraquat-Induced Apoptosis in PC12 Cells

Abstract

Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease. This study was aimed at investigating the neuroprotective mechanisms of the ethyl acetate fraction of Terminalia chebula ethanol-soluble extract using PC12 cells treated with paraquat as a model system. The ethyl acetate fraction of T. chebula ethanol-soluble extract was prepared using 95% ethanol and ethyl acetate as described in our previous study. The neuroprotective potential of the ethyl acetate fraction of T. chebula ethanol-soluble extract was analyzed by evaluating the intracellular reactive oxygen species and calcium levels, apoptosis, caspase-3 and α-synuclein activities, as well as Bcl-2 and Bax expressions. The ethyl acetate fraction of T. chebula ethanol-soluble extract exhibited neuroprotective effects against paraquat-induced apoptosis in PC12 cells at concentrations ranging from 0.4 μg/mL to 0.6 μg/mL. The various neuroprotective mechanisms identified for the extract included reduction in reactive oxygen species levels; inhibition of increased calcium ion concentration; increased Bcl-2 expression; reduced Bax, caspase-3 and α-synuclein expression; and reduced nuclear shrinkage. This study elucidates the various mechanisms underlying the neuroprotective effects of the ethyl acetate fraction of T. chebula ethanol-soluble extract that may further aid the Parkinson’s disease pharmacological application of T. chebula.