In conclusion, this study showed: (i) the potential therapeutic use of HRW for treating nerve injury-induced CNP and the associated emotional deficits, (ii) the activation of the endogenous antioxidant system and KATP channels as possible mechanisms of action of HRW in inhibiting neuropathic pain, (iii) a positive interaction between HO-1 and H2 systems in modulating nerve-injury induced neuropathy and (iv) the antioxidant, antinociceptive, anti-inflammatory and/or antiapoptotic actions of treatment with HRW in the DRG and/or AMG of mice with CNP. This evidence concerns the gene CNP and neuropathy.