The activation of NOD2 signaling in peripheral macrophage mediates the development of neuropathic pain through the production of pronociceptive cytokines (tumor necrosis factor and IL-1β).
Collectively, we proposed oxyntomodulin to attenuate TNF‑α induced neuropathic pain associated with the release of glial cytokines IL‑6 and IL‑1β via inhibiting the activation of the NF‑κB pathway.
Knockdown of ANXA10 at the spinal cord level suppressed the SNL-induced hyperalgesia and blocked the activation of NF-κB, TNF-α and IL-1β both in the early and late phase of NP.
Long-term actions of interleukin-1β on K<sup>+</sup>, Na<sup>+</sup> and Ca<sup>2+</sup> channel currents in small, IB<sub>4</sub>-positive dorsal root ganglion neurons; possible relevance to the etiology of neuropathic pain.
The aim of this study was to evaluate the role of the biomarker interleukin-1beta (IL-1ß) in the pharmacological interaction of gabapentin with tramadol in a model of diabetic neuropathic pain.
Additionally, we examine whether inhibiting LFA-1 or IL-1β actions in the spinal cord (intrathecal; i.t., route) could alleviate chronic neuropathic pain and reduce spinal and DRG glial activation markers, proinflammatory cytokines, and elevate anti-inflammatory cytokines.
In conclusion, our study indicated that 2 Hz EA reduces SNI-induced mechanical hypersensitivity via upregulating α7nAChR and downregulating IL-1β and CD11b in the spinal cord of SNI rats, which might be one of the mechanisms underlying its effectiveness in the neuropathic pain.
These data indicate that the upregulation of Cav2.2 in uninjured DRG neurons via IL-1β over-production contributes to neuropathic pain by increasing neuronal excitability following peripheral nerve injury.
These 2 P2XR subtypes differ pharmacologically and functionally: 1) P2X4Rs are activated at lower (≤0.1 mM) whereas P2X7Rs - at higher (≥1.0 mM) ATP concentrations; 2) P2X4R activation contributes to the release of brain derived neurotrophic factor and its role in tactile allodynia and neuropathic pain is demonstrated; 3) Due to its role in the secretion of pro-inflammatory IL-1β, P2X7Rs have been implicated in the development of neurodegenerative pathologies, pain and morphine tolerance.
Neuroinflammation, characterized by activation of spinal glial cells and increased production of pro-inflammatory cytokines (for example, IL-1β, TNF-α and IL-6), is a pathophysiological process closely related to neuropathic pain.
We previously reported that interleukin-1β (IL-1β) in the red nucleus (RN) is involved in pain modulation and exerts a facilitatory effect in the development of neuropathic pain.
Here, we explored the analgesic effects of PII on a model of CCI-induced NP and investigated the levels of the GFAP protein and the mRNA and protein levels of pro-inflammatory cytokines in the spinal cord, including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α).
Interleukin-1β pre-treated bone marrow stromal cells alleviate neuropathic pain through CCL7-mediated inhibition of microglial activation in the spinal cord.
Finally, intracisterna magna injection of interleukin-1 (IL-1) receptor antagonist reversed allodynia, implicating the pro-inflammatory cytokine IL-1 in the maintenance of neuropathic pain induced by facial nerve CCI.
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.