Diosgenin is a steroidal saponin extract from numerous plants, including Solanum and Dioscorea species, and has been reported to possess neuroprotective activity. However, the role of diosgenin in neuropathic pain remains unclear. The present study examined the effects of diosgenin on allodynia and the levels of inflammatory mediators in rats following neuropathic pain evoked by chronic constriction injury (CCI). In addition, the underlying molecular mechanisms involved in diosgenin‑induced suppression of neuropathic pain were examined. The results of the present study demonstrated diosgenin reversed CCI‑decreased mechanical withdrawal threshold and thermal withdrawal latency. Furthermore, diosgenin inhibited CCI‑induced upregulated levels of the pro‑inflammatory cytokines tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑2, and suppressed oxidative stress induced by CCI in the spinal cord. Furthermore, diosgenin significantly inhibited the expression of phosphorylated‑p38 mitogen activated protein kinase (MAPK) and nuclear factor (NF)‑κB in the spinal cord in CCI rats compared with sham‑operated rats. In conclusion, the present study demonstrated that diosgenin attenuates neuropathic pain in CCI rats by inhibiting activation of the p38 MAPK and NF‑κB signaling pathways. These results implicate diosgenin in the treatment of neuropathic pain, which merits further clinical investigation.
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