Subjective pain (assessed by visual analogue scale in pain diary and by chairside archwire activation), periodontal status (assessed by periodontal clinical parameters), cytokines in gingival crevicular fluid (interleukin 1β, prostaglandin E<sub>2</sub>, substance P) and periodontopathic bacteria (Porphyromonas gingivalis and Treponema denticola) in supragingival plaque were assessed.
Painful (mechanical and thermal hypersensitivity, ongoing pain and arthritis score) and inflammatory (oedema, plasma extravasation, cell infiltration and IL-1β release) parameters were assessed several hours after intra-articular injection of MSU (100 µg/articulation) in wild-type or knockout mice for Toll-like receptor 4 (TLR4), inducible nitric oxide synthase (iNOS), transient receptor potential (TRP) V1 and the IL-1 receptor (IL-1R).
Interleukin-1β is a potent proinflammatory cytokine that plays a key role in the pathogenesis of the brain aging and diverse range of neurological diseases including Alzheimer's disease, Parkinson's disease, stroke and persistent pain.
Since changes in AP shape facilitated Ca<sup>2+</sup> influx, this explains how IL-1β facilitates synaptic transmission in the dorsal horn; thereby provoking pain.
Oxyntomodulin was observed to attenuate TNF‑α‑induced pain hypersensitivity in mice, as well as the expression of IBA1, NF‑κB p‑p65, IL‑6 and IL‑1β in the spinal cord.
The main findings of this study indicate a functional network in which several IL-1β-related molecules in CSF influence fatigue in addition to the classical clinical factors of depression and pain.
Finally, intravenous injection of interleukin-1beta that induces pain hypersensitivity and memory deficits mimicked the SNI-induced the differential regulation of GSK-3β/β-catenin/BDNF in spinal dorsal horn and in hippocampus.
We have previously reported that chondroitin sulfate extracted from Sturgeon bone (CSSB) can alleviate the pain caused by osteoarthritis (OA) by reducing the expression of matrix metalloproteinases (MMPs) and inflammatory factors (IL-1, TNF-α and PGE<sub>2</sub>).
They constitute the main source of pro-inflammatory cytokines and chemokines such as TNF and IL-1β, they activate a wide range of immune and non-immune cells, and they secrete diverse tissue degrading enzymes driving chronic pro-inflammatory, tissue destructive and pain responses in RA.
Prolonged postsurgical pain was associated with increased expression of inflammatory genes, including those encoding Toll-like receptor 4, NOD like receptor protein 3 (NLRP3), nuclear factor kappa B (NFκB), caspase-1, interleukin-1β, and tumor necrosis factor (P < .05).
The repeated treatment of SCI-mice with MR309 resulted in significant pain behavior attenuation beyond the end of the administration period, accompanied by reduced expression of central sensitization-related mechanistic correlates, including extracellular mediators (TNF-α and IL-1β), membrane receptors/channels (NR2B-NMDA) and intracellular signaling cascades (ERK/pERK).
Interleukin-1β (IL-1β), tumor necrosis factor α (TNFα), and IL-6 expression were robustly increased in the DH of mice with EAE manifesting pain, whereas these cytokines showed a modest increase or no change in mice with EAE in the absence of pain.
Thus, we investigated whether miR-187-3p is involved in the pathogenesis of IR-induced pain hypersensitivity by regulating the P2X7R signal and subsequent IL-1β release.
Intravenous injection of clodronate liposomes depleted synovial macrophages, which decreased the level of not only proinflammatory mediator interleukin-1β but also NGF in the knee joint, leading to pain suppression in the advanced OA model.
Given that selective inhibition of NLRP3 alleviates postoperative mechanical pain, its selective targeting may be a novel and effective strategy for the treatment of pain that would avoid complications of global IL-1β inhibition.
Regression analysis-based results reflected no significant association between increasing self-rated pain and whole salivary IL-1β, IL-6, and TNF-α levels.
Moreover, Cel-Indo-NLCs showed prominent effect of decreasing paw oedema, inhibiting inflammation and pain by regulating the levels of IL-1β, TNF-α, β-endorphin and Substance P. After the administration of Cel-Indo-NLCs-gel, no skin irritation was observed in rats.
Physiological parameters (heart rate, respiratory rate, rectal temperature, invasive blood pressure, cortisol, β-endorphin, interleukin-1β, interleukin-6, tumor necrosis factor-α and haptoglobin plasmatic concentration), local variables (tactile sensitivity score, pressure pain thresholds and horn temperature), behavior and pain scores [multidimensional pain scale and visual analogue scale (VAS)] were assessed at baseline and at several pre-determined time points until 24h after disbudding.
These results suggest that minocycline provides protection against neonatal systemic LPS exposure-induced enhanced pain sensitivity (allodynia and hyperalgesia), and that the protective effects may be associated with its ability to attenuate LPS-induced microglia activation, and the levels of IL-1β, COX-2, and PGE2 in the spinal cord of neonatal rats.