A single 10 μM low dose of controlled release mAv-Dex (2:1:1) effectively suppressed IL-1α-induced GAG loss, cell death and inflammatory response significantly better than unmodified Dex over 2 weeks in cartilage explant culture models of OA.
CONCLUSIONS Our work suggested that catalpol treatment attenuates IL-1ß-induced inflammatory response and catabolism in rat chondrocytes by inhibiting the NF-kappaB pathway, suggesting the therapeutic potential of catalpol for the treatment of osteoarthritis.
MATERIAL AND METHODS To explore the potential therapeutic effect of leonurine against osteoarthritis (OA), rat chondrocytes were treated with IL-1ß along with different concentrations of leonurine in vitro.
Membrane-Free Stem Cell Components Inhibit Interleukin-1α-Stimulated Inflammation and Cartilage Degradation in vitro and in vivo: A Rat Model of Osteoarthritis.
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.
MATERIAL AND METHODS To clarify the roles of loganin in OA and its specific signaling pathway, chondrocytes were administrated with IL-1ß and supplemented with or without LY294002 (a classic PI3K/Akt inhibitor).
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>).
Here, interleukin-1 signaling (IL-1) plays a central role and its effects on the different cell types involved in OA are discussed in this review with a special focus on the chondrocyte.
Biomarkers of inflammation and cartilage degradation related to OA were also analyzed and significant differences were detected only for IL1-α, which decreased in the MD group.
OA-induced IL-1α release was significantly (P < 0.05) reduced following red LED light at 0.2, 0.5, and 1.2 J/cm<sup>2</sup> , from 266 ± 11 pg/ml of no-light-plus-OA-treated (OA treatment without light) controls to 216 ± 9, 231 ± 8, and 212 ± 7 pg/ml, respectively.
Additionally, geniposide markedly suppressed the expression of IL-1, TNF-<i>α</i>, NO, and MMP-13 in the synovial fluid from the rabbits with osteoarthritis.
These findings suggest that the elevated levels of IL-1α found in the OA environment heighten FLS sensitivity to fluid shear by altering both intercellular communication and individual cell sensitivity, which could affect downstream functions and contribute to progression of the disease state.
Safety, tolerability, and pharmacodynamics of an anti-interleukin-1α/β dual variable domain immunoglobulin in patients with osteoarthritis of the knee: a randomized phase 1 study.
We investigated IL-1-induced regulation of genes related to inflammation and atherogenesis in human keratinocytes and endothelial cells, and if 'diacerein', an oral IL-1 inhibiting drug currently approved for use in osteoarthritis, would reverse IL-1's effects on these cells.
IL-1α and IL-1β are not involved in synovial inflammation and cartilage destruction during CiOA, implicating that other mediators are responsible for the joint damage.
The increase in miR-365 expression in OA cartilage and in response to IL-1 may contribute to the abnormal gene expression pattern characteristic of OA.
The present study aimed to identify the association between an insertion/deletion (Ins/Del) polymorphism (rs3783553) in the 3'‑untranslated region (3'‑UTR) of interleukin‑1α (IL‑1A) and the risk for osteoarthritis (OA).
Our results indicate that IL-6, IL-1A, and IL-1B genetic polymorphisms are statistically correlated with an increased risk of OA under the allele and dominant models.
Furthermore, OSM also increased expression of its own receptors, gp130 and OSMR and the IL-1 receptor, IL1-R1; the latter effects were also observed in both human OASFs and RASFs.
Using rabbit and human synovial fibroblast cell lines, we examined the effects of Cx43 overexpression and Cx43 siRNA-mediated knockdown on the gene expression of OA-associated matrix metalloproteinases (MMP1 and MMP13), aggrecanases (ADAMTS4 and ADAMTS5), and inflammatory factors (IL1, IL6 and PTGS2) by quantitative real time RT-PCR.