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.
In vitro, expressions of OA-related factors and NF-κB transcriptional activation were down-regulated by GRK5 gene suppression in human OA chondrocytes (3.49-fold decrease in IL6, p < 0.01; 2.43-fold decrease in MMP13, p < 0.01; and 2.66-fold decrease in ADAMTS4; p < 0.01).
The results showed that, compared to the OA group, the OA + treadmill and OA + wheel groups had lower levels of IL-1β, IL-6 and TNF-α, and similar levels of p-P65, p-JNK, and P-IκBα.
At 2 months post-surgery, intra-articular evidence of CTXII, IL1β, IL6, TNFα, and IFNγ was evaluated using a multiplex magnetic capture technique, and histological evidence of OA was assessed via a quantitative histological scoring technique.<b>Results</b>: Elevated levels of CTXII and IL6 were found in MCLT+MMT knees relative to skin-incision and contralateral controls; however, animal age did not affect the severity of joint inflammation.
In addition, MPE suppressed IL-1β (60.9%), TNF-α (37.9%) and IL- 6 (40.9%) production and suppressed the synthesis of MMP-2, MMP-9 and COX-2 in the MIA-induced OA rat model.
We found that GANT-61 and indomethacin synergistically attenuate cartilage damage and serum levels of inflammatory cytokines TNF-α, IL-2 and IL-6 in OA mice.
In both OA-model groups immunohistochemistry and qPCR showed a significantly increased expression of MMPs and IL6 compared to their respective control group.
The cytokines, such as interleukin 1 (IL-1), IL-6, IL-17, tissue inhibitor of metalloproteinase-1 (TIMP-1) and matrix metalloproteinase (MMPs), involved in the degradation of chondrocyte in CILinc02 knockdown OA primary cells, which were treated with methylene blue that were determined by enzyme-linked immunosorbent assay, qRT-PCR and Western blot analysis.
The inflammatory pattern was assessed by RT-qPCR and ELISA (interleukin 6 (IL-6), IL-8, Cox2, and prostaglandin E2 (PGE<sub>2</sub>)) after a 24-h stimulation by IL-1β (1 ng/mL) and by conditioned medium from OA synovium.
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.
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).
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.
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.
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.
Results showed that high doses of PM (5 mg) significantly increased pro-inflammatory factors such as tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and IL-6, and M1 macrophages in the lung region, also obtained in systemic IL-6 and TNF-α expressions in this MIA-OA rat model.
Long Non-Coding RNA (LncRNA) CAIF is Downregulated in Osteoarthritis and Inhibits LPS-Induced Interleukin 6 (IL-6) Upregulation by Downregulation of MiR-1246.
The results demonstrated that CH inhibited cell apoptosis, dose‑dependently reduced matrix metalloproteinase (MMP) 13, collagenase and IL‑6 expression, and increased collagen α‑1 (II) chain (COL2A1) expression in human osteoarthritis chondrocytes.
Though several pro-inflammatory cytokines, chemokines and growth factors present in the 30plex magnetic bead panel were not significantly (p>0.05) increased in the plasma of RA patients, the levels of plasma Th1 associated proinflammatory cytokines TNFα, and IL-6 and Th2 associated cytokines such as IL-4, IL-5 and IL-13 were significantly (p<0.05) upregulated compared to OA and normal controls.
Human OA chondrocytes were pretreated with juglanin (10, 20 and 40 μM) for 2 h and subsequently stimulated with IL-1β for 24 h. Nitric oxide (NO) production was determined using the Griess method and prostaglandin E2 (PGE2), matrix metalloproteinase-3, -9 and -13 (MMP-3, MMP-9 and MMP-13), TNF-α, and IL-6 were assessed using ELISA.
The purpose of this study was to investigate the influence of moderate physical activity (MPA) on the expression of osteoarthritis (OA)-related (IL-1β, IL-6, TNF-α, MMP-13) and anti-inflammatory and chondroprotective (IL-4, IL-10, lubricin) biomarkers in the synovium of an OA-induced rat model.