Antinociception induced by rosuvastatin in murine neuropathic pain

Abstract

Background: Neuropathic pain, and subsequent hypernociception, can be induced in mice by paclitaxel (PTX) administration and partial sciatic nerve ligation (PSNL). Its pharmacotherapy has been a clinical challenge, due to a lack of effective treatment. In two models of mouse neuropathic pain (PTX and PSNL) the antinociception induced by rosuvastatin and the participation of proinflammatory biomarkers, interleukin (IL)-1 beta, TBARS and glutathione were evaluated. Methods: A dose-response curve for rosuvastatin ip was obtained on cold plate, hot plate and Von Frey assays. Changes on spinal cord levels of IL-1 beta, glutathione and lipid peroxidation were measured at 7 and 14 days in PTX and PSNL murine models. Results: PTX or PSNL were able to induce in mice peripheral neuropathy with hypernociception, either to 7 and 14 days. Rosuvastatin induced a dose dependent antinociception in hot plate, cold plate and Von Frey assays. The increased levels of IL-1 beta or TBARS induced by pretreatment with PTX or PSNL were reduced by rosuvastatin. The reduction of spinal cord glutathione, by PTX or PSNL, expressed as the ratio GSH/GSSG, were increased significantly in animals pretreated with rosuvastatin. The anti-inflammatory properties of statins could underlie their beneficial effects on neuropathic pain by reduction of proinflammatory biomarkers and activation of glia. Conclusion: The findings of this study suggest a potential usefulness of rosuvastatin in the treatment of neuropathic pain.