The analgesic actions of both compounds were mainly produced by inhibiting apoptotic responses, and activating the endogenous antioxidant system by triggering the synthesis of antioxidant enzymes—such as superoxide dismutase 1 (SOD-1), glutathione S-transferase Mu 1 (GSTM1), heme oxygenase 1 (HO-1), and quinone oxidoreductase 1 (NQO1)—in the amygdala (AMG) and periaqueductal gray matter (PAG) of mice with nerve-injury-induced neuropathy [23]. Here, SOD1 is linked to neuropathy.