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.
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.
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%).
Among them, we evidence that amentoflavone showed very favorable interactions with the enzyme COX-2 in the in silico analysis.Thus, it is concluded that <i>A. chica</i> has important analgesic properties for the treatment of OA.
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.
Etodolac is a nonsteroidal anti-inflammatory drug with selective cyclooxygenase-2 inhibition to treat pain and inflammation associated with osteoarthritis in humans and dogs.
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.
In vitro and in vivo studies demonstrated that CJM reduced the IL-1β-, IL-6, IL-17- and TNF-α-induced up-regulation of MMP3, MMP13, ADAMTS4, ADAMTS5 and COX-2 and blocked osteoarthritis development in a destabilization of the medial meniscus mouse model.
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.
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.
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).
ELF3 levels are elevated in human cartilage from patients with osteoarthritis (OA), and ELF3 contributes to the IL-1β-induced expression of genes encoding Mmp13, Nos2, and Ptgs2/Cox2 in chondrocytes in vitro.
Curcuminoids were found to have anti-inflammatory properties by inhibiting Cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) enzyme and hence have potential application in the treatment of Osteoarthritis (OA).
Vitacoxib, a selective COX-2 inhibitor, is approved for the relief of pain and inflammation associated with orthopedic surgery and osteoarthritis in dogs.
Our results demonstrated that sauchinone significantly attenuated NO and PGE2 production, as well as inhibited iNOS and COX-2 expression in IL-1β-stimulated OA chondrocytes.
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.
After multi‑induction, hUC‑MSCs were able to differatiate into adipogenic, osteogenic and chondrogenic lineage. hUC‑MSCs inhibited the expression of matrix metalloproteinase‑13, collagen type X α1 chain and cyclooxygenase‑2 in OA chondrocytes, and enhanced the proliferation of OA chondrocytes, while OA chondrocytes stimulated the production of Col2, sox‑9 and aggrecan and promoted hUC‑MSCs differentiate into chondrocytes.
At present, steroidal drugs and nonsteroidal anti-inflammatory drugs (NSAIDS), selective cyclooxygenase-2 (COX-2) inhibitors, are the first-line drugs for the treatment of OA.
Exposure to oral OA therapies (acetaminophen, non-steroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase-2 (COX-2) inhibitors, narcotics, and glucosamine/chondroitin sulfate) was determined within the 3 years prior to the date of the KR.