Vitacoxib, a selective COX-2 inhibitor, is approved for the relief of pain and inflammation associated with orthopedic surgery and osteoarthritis in dogs.
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.
To evaluate the in vitro effects of diacerhein, a new drug for the treatment of osteoarthritis (OA), and its active metabolite, rhein, on the production of nitric oxide (NO), prostaglandin (PGE2), cyclooxygenase-2 (COX-2), as well as the production and expression of the inducible nitric oxide synthase (iNOS) in human OA chondrocytes.
This study revealed that the cartilage protective effect of osthole in a MIA-induced osteoarthritis (OA) murine model can be explained by downregulation of COX-2 and RUNX2 by inhibition of NF-κB and HIF-2α up-regulated by OA induction, resulting in downregulation of MMP-13, Syndecan IV and ADAMTS-5.
This study investigated whether 14 days of the selective Cox-2 inhibitor etoricoxib (60 mg/day) would modify self-report of pain intensity and quality, and physical measures of hyperalgesia and function in individuals with knee OA.
This study elucidates the detailed mechanism of low shear stress regulating the resistin-induced catabolic COX-2 expression and indicates a possible reparative role of moderate shear force in resistin-stimulated OA development..
Therefore, we evaluated the disease-modifying effects and the optimal dose of polyesteramide microspheres delivering the COX-2 inhibitor celecoxib in a rat OA model.
The use of COX-2 inhibitors in OA was associated with a significant increased risk of drug-related AEs compared with placebo (relative risk (RR) 1.26, 95% CI 1.09-1.46; I<sup>2</sup> = 24%).
The results demonstrated that hesperidin treatment markedly decreased nitric oxide and prostaglandin E2 production and markedly downregulated inducible nitric oxide synthase and cyclooxygenase-2 expression in IL-1β-stimulated OA chondrocytes.
The highest inhibition of cyclooxygenase 2 in the crude extract occurred at 50 µg/mL.The crude extract of <i>S. dulcis</i> presents therapeutic potential for the treatment of osteoarthritis due to its anti-inflammatory and anti-nociceptive action.
The expression of COX-2, but not the expression of COX-1, was found to be elevated in a disease-related pattern in the synovial tissue from patients with RA, AS, or PsA in comparison with OA samples, and was especially high in AS synovial tissue.
The authors performed further measurements of MMP-13 production in osteoarthritis chondrocytes stimulated by the EP2 agonist butaprost in the presence or absence of interleukin-1β (IL-1β) and/or cyclooxygenase-2 (COX-2) inhibitor.
The aim of this study, was to describe the effect of a multistrain probiotic (PB) and chondroitin sulfate (CS), administered separately or in combination, on the expression of Ptgs2, Tgfb1 and Col2a1 during monoiodoacetate-induced OA in male rats.
The aim of the current study is to evaluate the effects of escin on cyclooxygenase-2 (COX-2, isoform), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), interleukin-18 (IL-18), tumor necrosis factor-alpha (TNF-α), and nitric oxide (NO) (1), as well as prostaglandin E2 (PGE2) on inflammatory cells, similar osteoarthritis in synoviocytes, and monocytes/macrophages, and to compare it with dexamethasone (DEX) and ibuprofen (IBP).
Targeted and untargeted metabolomics were used to investigate the effect of COX-2 deletion or inhibition in mice and in osteoarthritis patients exposed to nonsteroidal anti-inflammatory drugs on the l-arginine/nitric oxide pathway.
PPAR-mediated induction of COX-2 expression and synthesis in human OA synovial fibroblasts is inhibited by therapeutic concentrations of NIM through the functional antagonism of ligand-dependent receptor activation, with the resultant suppression of PPAR-dependent transactivation of target genes (e.g., COX-2).
Patients who have OA and T2DM receiving combination COX-2 inhibitors and metformin therapy associated with lower joint replacement surgery rates than those without and this may be attributable to combination therapy much more decrease pro-inflammatory factors associated than those without metformin therapy.
Our results revealed that miR-26a-5p was poorly expressed, while PTGS2 was highly expressed in OA patients and synovial fibroblasts treated with IL-1β.