Gene expression was determined at baseline and after fibroblast stimulation with tumor necrosis factor-α (TNF), modeling inflammation as a common pain trigger in FD.
We observed that antibiotics treatment-prolonged nitroglycerin (NTG)-induced acute migraine-like pain in wild-type (WT) mice and the pain prolongation was completely blocked by genetic deletion of tumor necrosis factor-alpha (TNFα) or intra-spinal trigeminal nucleus caudalis (Sp5C) injection of TNFα receptor antagonist.
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).
The control mice were intrathecally injected with tumor necrosis factor-α (TNF-α) and lipopolysaccharide, the bone cancer pain mice were intrathecally injected with the endoplasmic reticulum stress inhibitors 4-PBA and GSK2606414.
To assess the suitability of these markers in SAH, we evaluated the courses of corticosterone, IL-6 and TNF-α up to 6h in an acute model simulating SAH in continuously anaesthetized rats, lacking the pain and stress induced impact on these parameters.
Tumor necrosis factor (TNF) is a proinflammatory cytokine, which is involved in physiological and pathological processes and has been found to be crucial for pain development.
In the present study, intraperitoneal injection of Tα1 attenuated complete Freund's adjuvant (CFA)-induced pain hypersensitivity, and decreased the up-regulation of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in inflamed skin and the spinal cord.
In this study, we investigated whether SP is involved in inflammatory orofacial pain by upregulating interleukin (IL)-1β and tumour necrosis factor (TNF)-α from SGCs, and we explored whether MAPK signalling pathways mediate the pain process.
In the present study, we aimed to determine whether serum levels of TNFα during therapy with TNFα inhibitors do really reflect the disease activity and correspond to the intensity of pain experienced.
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>).
Both SFKs and p38 inhibitors alleviated pain behaviors in a dose-responsive manner without disturbing locomotor function and reduced spinal expression of TNF-α, IL-1β, and IL-6 in rats with NP.
Also, the expression of these miRNAs was significantly correlated with that of IL-6, TNF-α, and COX-2, which have been shown to mediate pain intensity in patients with CFS.
Through causal mediation analyses, the proportion of the effect of a 18 months diet and exercise intervention explained by the 18 months change in interleukin (IL)-6, TNF-α, soluble IL-6 receptor, soluble IL-1 receptor, CRP, and BMI were assessed, using self-reported pain and function as outcomes.
There are no studies that have evaluated the correlation between self-rated pain, peri-implant clinical and radiographic parameters (plaque index [PI], bleeding on probing [BOP], probing depth [PD], and crestal bone loss [CBL]) and whole salivary interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) levels among patients with and without peri-implantitis.
This mechanism is used in the treatment of pain in diabetic peripheral neuropathy) pretreatment or by inhibition of TNF-α with Etanercept (ETA), administered up to 7 days prior to NE or within 24 h of noise.
Systemic inflammation with high levels of pro-inflammatory cytokines (Eotaxin, IL-1β, IL-7, IL-8, IL-12/IL-23p40, IL-12p70, IL-13, IL-16, IP-10, MCP-1, MCP-4, MDC, MIP-1a, TARC, TNFß) was associated with diminished quality of life in general and specific domains including pain, physical and cognitive functioning.
The finding that FLX improved depressive behavior and pain through normalized 5-HT concentrations and TNF-α mRNA expression establishes the initial mechanism of the comorbidity of pain and depression.
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.
Our preliminary non-randomized controlled pilot study to examine the effects of high-intensity aerobic exercise on progesterone, prostaglandin metabolite (13,14-dihydro-15-keto-prostaglandin F2 alpha (KDPGF<sub>2α</sub>), TNF-α, and pain intensity found increases in progesterone and decreases in KDPGF<sub>2α</sub>, TNF-α, and pain intensity following high-intensity aerobic exercise relative to no exercise.
This post hoc analysis included assessment of spinal and nocturnal back pain, FACIT-Fatigue, and association between pain and either FACIT-Fatigue or ASQoL item 5 (sleep quality) for the approved secukinumab 150 mg dose in the overall population, and stratified by baseline high-sensitivity C-reactive protein (hsCRP) levels (normal [<5 mg/L] or elevated [≥5 mg/L]) or prior TNF inhibitor therapy status (TNFi-naïve or inadequate response [TNFi-IR]).
The objectives of the present study were to determine the effects of B1 (<i>N</i>-[(1<i>H</i>-benzimidazol-2-yl)methyl]-4-methoxyaniline) and B8 (<i>N</i>-{4-[(1<i>H</i>-benzimidazol-2-yl)methoxy]phenyl}acetamide), benzimidazole derivatives, on thermal nociception and mechanical allodynia during repeated morphine (intraperitoneal; 5 mg/kg twice daily for 6 days)-induced paradoxical pain and TNF-α expression in the spinal cord in mice.