Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In contrast, in osteoarthritis FLSs only one gene, that for IL-6, was modulated.
|
15642131 |
2005 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Signalling molecules (such as STAT3, FOXP3) were highly expressed in PsA SFCs, while cytokines (such as IL17F, IL6) were more predominant in OA SFCs after non-supervised hierarchal clustering.
|
29148410 |
2018 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In patients with RA, mRNA expression of IL-6, but not TNFalpha and IL-1beta, in the cancellous bone and IL-6 and PGE2 production in the osteoblast-lineage cells were significantly higher than in patients with OA.
|
11281165 |
2001 |
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Gain- and loss-of-function studies revealed that FoxC1 overexpression promoted, whilst silencing inhibited OA synovial fibroblast (OASF) proliferation and pro-inflammatory cytokine (interleukin 6 (IL-6), interleukin 8 (IL-8), and tumour necrosis factor-α (TNF-α)) production.
|
31837247 |
2019 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
LHGDN |
Synovial fluid IL-6 levels may help to classify OA patients and may point to a subgroup with a particular impact from their immune system.
|
17476620 |
2007 |
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, articular cartilage tissues in knee OA patients have higher levels of MMP-9 and IL-6 expression, and these may play a synergistic role in OA pathogenesis.
|
26600476 |
2015 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In vitro, UA inhibited the interleukin-1 beta (IL-1β) induced over-production of nitric oxide (NO), prostaglandin E<sub>2</sub> (PGE<sub>2</sub>), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in a concentration-dependent manner in human OA chondrocytes.
|
31497826 |
2019 |
Degenerative polyarthritis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The level of histone H3 acetylation (H3ac) in the IL-6 promoter was significantly higher in RASFs than osteoarthritis (OA) SFs.
|
24513290 |
2014 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Systemic blockade of IL-6 by MR16-1 alleviated DMM-induced OA cartilage lesions, impaired the osteophyte formation and the extent of synovitis.
|
27789465 |
2017 |
Degenerative polyarthritis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Compared with the OA group, the IL-1β (153.11 ± 16.05 pg mg<sup>-1</sup>), IL-18 (3.71 ± 0.7 pg mg<sup>-1</sup>), IL-6 (14.15 ± 1.94 pg/mg) and TNF-α (40.45 ± 10.28 pg mg<sup>-1</sup>) levels in H-DEX group were decreased (<i>p</i> < 0.05).
|
31545916 |
2019 |
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Q-PCR methods were validated by demonstrating increased expression of IL-1beta and IL-6 expression in rheumatoid arthritis synovial samples compared with osteoarthritis synovium.
|
14680510 |
2003 |
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Here, we used an in vitro model of inflammation in osteoarthritis (OA) to investigate the potential of PE to suppress interleukin 1 beta (IL-1β)-stimulated expression of inflammatory cytokine IL-6, generation of reactive oxygen species (ROS) levels, and investigated the mechanism of NF-κB inhibition by analyzing the activation of the kinases upstream of IκBα in primary human chondrocytes.
|
28276100 |
2017 |
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The present study was undertaken to investigate whether ZCCHC6 directs the expression of IL-6 and influences OA pathogenesis in vivo.
|
30302948 |
2019 |
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We investigated whether SAHA suppresses the expression of IL-6 by perturbing the miR-9-MCPIP1 axis in OA chondrocytes under pathological conditions.
|
27404795 |
2017 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We conducted a secondary data analysis of a dataset containing alternate Healthy Eating Index-2010 (AHEI-2010), body composition, OA severity, and serum interleukin-6 (IL-6) data from 126 AA females (aged 60⁻87 years) with OA to examine the relationships between these variables.
|
30583501 |
2018 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The therapeutic effects of treatment groups [concentration of interleukin-6 (IL-6) in blood serum, radiographic and the histological grading on articular joint] were compared with those of normal saline treated OA and normal rats.
|
28251487 |
2017 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Osteoarthritis (OA) is a degenerative condition that involves the production of inflammatory cytokines (e.g., interleukin-1β (IL-1β), tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6)) that stimulate degradative enzymes, matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS) resulting in articular cartilage breakdown.
|
31434236 |
2019 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, proteomics has displayed that some pro-inflammatory cytokines, namely IL-6, IL-8 and IL-18, have a role in OA.
|
30644275 |
2019 |
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In this study, we found that silibinin significantly inhibited the nterleukin-1β (IL-1β)-induced production of nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α) and IL-6, expression of cyclooxygenase2 (COX-2), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-1 (MMP-1), MMP-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4) and ADAMTS-5, degradation of aggrecan and collagen-II in human OA chondrocytes.
|
29245931 |
2017 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Synovial fluid (SF) mononuclear cells (MNC) from 13 patients with rheumatoid arthritis (RA) and 12 patients with other arthritic diseases (OD) including osteoarthritis (OA), gout and spondyloarthritis (SA) were cultured in the presence of collagen types I and II or lipopolysaccharide (LPS) for 24 h. Interleukin-1 (IL-1), IL-6 and tumor necrosis factor-alpha (TNF-alpha) in the SF and culture supernatants were assayed using ELISA.
|
7622181 |
1995 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
TXC treatment reversed cartilage degeneration related biomarkers (ADAMTS 4, ADAMTS 5, Col I, Col V, MMP 3, MMP 9, and MMP 13) and inflammation factors (IL-1β, TNF-α, and IL-6) in both the animal and cellular OA models.
|
31760158 |
2020 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In vitro, PD treatment completely suppressed the over-production of pro-inflammatory mediators, including prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), nitric oxide (NO), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and IL-6 in IL-1β-induced human OA chondrocytes.
|
29484338 |
2018 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Vitamin E also significantly (<i>p</i> < .05) inhibited MIA+STZ-induced blood levels of the inflammatory biomarkers, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) that are known to be modulated in OA and diabetes.
|
31177887 |
2019 |
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
ELISA results demonstrated that the proinflammatory cytokine levels of interleukins-6 (IL-6) and tumour necrosis factor α (TNF-α) in the serum and synovial fluid and HIF-1α level in the synovial fluid were significantly elevated in OA patients compared to normal healthy subjects.
|
31055848 |
2019 |
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, overexpression of miR-138 suppressed the protein levels of p65, COX-2 and IL6 in human OA chondrocytes and chondrogenic SW1353 cells.
|
28537665 |
2017 |