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1), as has previously been demonstrated in cell-free extracts of D

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This implies sodium channel inhibition, a blockade of voltage-gated sodium channels (VGSCs) leading to a reversible block of action potential propagation [278], and reduced permeability of cell membranes, thereby blocking depolarization and preventing the conduction of the electrical impulse through which pain occurs [279]

The protection against MPP-induced neurotoxicity was associated with activation of Nrf2 pathway (a crucial defense mechanism against oxidative stress), via the ERK1/2 signaling pathway [57], inhibition of the mitochondrial ROS-dependent oxidative stress, and enhancement of the Erk1/2/Drp1 and Fak/Akt/GSK3 signaling pathways [104]