Collectively, lidocaine promoted the SOCS3 expression in microglia, in turn leading to suppression of IBA1<sup>+</sup> microglia accumulation and p38 MAPK and NF-κB, which may expand our understanding on lidocaine in suppressing neuroinflammation and neuropathic pain.
Our findings validated that MKP1 in the mPFC modulated chronic neuropathic pain via p38 and JNK1/2, suggesting a possible MKP1-mediated process would participate in neuronal transmission pathways implicated in pain modulation.
As p38 in the spinal microglia plays a critical role in neuropathic pain, we expect that p38 siRNA NPs could be a promising tool for the treatment of neuropathic pain.
We determined the effect of N-acetylcysteine (NAC) on the expression of the phosphorylated p38 (p-p38) protein and superoxide anion generation (SAG), two important players in the processing of neuropathic pain, in the lumbosacral spinal cord of rats with chronic constriction injury (CCI)-induced neuropathic pain.
CONCLUSIONS Our findings indicate that down-regulation of miR-128 in murine microglial cells may contribute to the development of NPP following SCI via activation of P38.
Taken together, our data suggest that CXCL13 acts on CXCR5 to increase p38 activation and further contributes to the pathogenesis of orofacial neuropathic pain.
These findings indicate that alendronate could effectively relieve chronic constriction sciatic nerve injury-induced neuropathic pain by at least partially inhibiting the activation of spinal microglia and the p38 MAPK signaling pathway.