Furthermore, we found that miR-129-5p alleviated neuropathic pain through downregulating high mobility group protein B1 (HMGB1) expression in CCI rats as overexpression of miR-129-5p suppressed expression of both HMGB1 and proinflammatory cytokine and alleviated pain sensation in CCI rats.
The current study aimed to characterize neuropathic pain-induced changes in affect over time and to determine whether HMGB1 has a role in neuropathic pain-induced changes in affect.
Since there is growing evidence that spinal MIF and HMGB1 mediate inflammatory and neuropathic pain we examined whether there were spinal changes occurring during persistent bladder pain that may be responsible for maintaining bladder pain.
Overall, these results suggest that miR‑142‑3p functions as a negative regulator of neuropathic pain development through the downregulation of HMGB1, indicating that miR‑142‑3p may serve as a potential therapeutic target for neuropathic pain.
Though it is known that dorsal root ganglia (DRG) sensory neurons exposed to HMGB1 and TLR4 agonists can influence excitation, the degree to which at-HMGB1 signaling through neuronal RAGE contributes to neuropathic pain is unknown.
Here, we overview the characteristics of HMGB1 as a pro-inflammatory mediator and show the promise of HMGB1 as a therapeutic target for neuropathic pain.