Our results showed that both IL-6 and Jun genes and the signaling pathway of MAPK, apoptosis, P53 present their vital modulatory role in nerve regeneration and neuropathic pain.
Overall, our data suggest the role played by exercise in improving neuropathic pain after STZ and that IL-6-mTOR signal is a part of mechanisms engaged in the effects of exercise.
Our results suggest that IL-6 upregulates Ca<sub>v</sub>3.2 T-type channels expression and function through the IL-6/sIL-6R trans-signaling pathway in DRG neurons, thus contributes to the development of neuropathic pain in SNL rats.
Our present findings highlighted that SNL caused pain hypersensitivity and increased the expression of spinal ANXA10/pNF-κB, TNF-α, IL-1β, and IL-6 both in the early and late phase of NP in rats, while spinal MMP-9 was only slightly increased in the early phase of NP.
Moreover, miR-144 negatively regulated neuroinflammation by decreasing the expression of proinflammatory mediators, including TNF-α (tumor necrosis factor-α), IL (interleukin)-1β, and IL-6, thus facilitating the inhibition of neuropathic pain development.
Inhibition of neuropathic pain by exercise in STZ rats was accompanied by decreases in interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α levels and downregulated expression of their receptors.
Thus, in this study we examined signaling pathways of interleukin-6 (IL-6) and transient receptor potential ankyrin 1 (TRPA1) in the sensory nerves responsible for neuropathic pain induced by BTZ and further determined if influencing the pathways can improve neuropathic pain.
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.
The MCP1 concentration in serum was associated with higher global pain ratings and increased spinal pressure pain sensitivity, while IL-6 serum concentration correlated with the intensity of the neuropathic pain component (leg pain) in LDH patients.
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.
Therefore, the present study aimed to evaluate the effectiveness of LLLT on neuropathic pain and interleukin-6 (IL-6) expression following SCI in male rats.
Activation of p38MAPK in spinal cord could downregulate the GR expression and thereby activate NF-κB, thus promoting the release of IL-6 and TNF-α and participating in the development of neuropathic pain.
These results suggest that RN IL-6 participates in the later maintenance of SNI-induced neuropathic pain and plays facilitated role through activating JAK/STAT3 and ERK signaling pathways.
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).
IL‑6, c‑Jun, and Plau may be involved in development of neuropathic pain and further research investigating the exact role of these key genes is required.
Overexpression of miR-93 significantly alleviated neuropathic pain development and reduced inflammatory cytokine expression, including interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6 in CCI rats.
Exercise Combined With Ultrasound Attenuates Neuropathic Pain in Rats Associated With Downregulation of IL-6 and TNF-α, but With Upregulation of IL-10.