Paeoniflorin attenuates the neuroinflammatory response in a rat model of chronic constriction injury

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Abstract

Neuropathic pain remains the most frequent cause of suffering and disability worldwide. Paeoniflorin (PF), a water-soluble monoterpene glycoside extracted from the roots of Paeonia lactiflora Pall, has a wide range of pharmacological functions. Although the neuroprotective effect of PF has been reported in animal models of neuropathology, no systematic investigation has reported on the analgesic properties of PF in neuropathic pain. The aim of the present study was to investigate whether PF can alleviate neuropathic pain and to examine its possible mechanism. Neuropathic pain was induced by chronic constriction injury (CCI) of the sciatic nerve in rats. Following CCI surgery, the rats were administered with PF for 11 days. Mechanical withdrawal threshold and thermal withdrawal latency were assessed prior to surgery, and on days 3, 7 and 11 post-surgery. The levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α in the spinal cord were analyzed using enzyme-linked immunosorbent assays. The activation of astrocytes and microglia were observed using immunostaining. In addition, the phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK) and nuclear factor-κB (NF-κB) were examined using western blot analysis. The results indicated that PF significantly attenuated CCI-induced neuropathic pain and decreased the levels of TNF-α and IL-1β proinflammatory cytokines in the spinal cord. Furthermore, PF inhibited the over-activation of microglia and reduced the elevated expression levels of p-p38 MAPK and NF-κB in the spinal cord. These results indicated that PF offers potential as a therapeutic agent for neuropathic pain, which merits further investigation.

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Zhou, J., Wang, J., Li, W., Wang, C., Wu, L., & Zhang, J. (2017). Paeoniflorin attenuates the neuroinflammatory response in a rat model of chronic constriction injury. Molecular Medicine Reports, 15(5), 3179–3185. https://doi.org/10.3892/mmr.2017.6371

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