The objective of this study was to explore the protective potential of caffeic acid phenethyl ester in paclitaxel-induced neuropathic pain.
We examined the effects of caffeic acid phenethyl ester by administering paclitaxel (2 mg/kg, intraperitoneal) to female Sprague Dawley rats on four alternate days to induce neuropathic pain, followed by the administration of caffeic acid phenethyl ester (10 and 30 mg/kg, intraperitoneally).
Rats that were administered paclitaxel showed a substantially diminished pain threshold and nerve functions after 28 days. A significantly increased protein expression of Wnt signalling protein (β-catenin), inflammatory marker (matrix metalloproteinase 2) and a decrease in endogenous antioxidant (nuclear factor erythroid 2-related factor 2) levels were found in paclitaxel administered rats in comparison to the naïve control group. Caffeic acid phenethyl ester (10 and 30 mg/kg, intraperitoneal) showed improvements in behavioural and nerve function parameters along with reduced expression of β-catenin, matrix metalloproteinase 2 and an increase in nuclear factor erythroid 2- related factor 2 protein expression.
The present study suggests that caffeic acid phenethyl ester attenuates chemotherapyinduced peripheral neuropathy via inhibition of β-catenin and matrix metalloproteinase 2 and increases nuclear factor erythroid 2-related factor 2 activation.