1995
DOI: 10.1016/s0021-5198(19)46262-8
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Effects of antiinflammatory agents on matrix metalloproteinase-3(MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1) production by human chondrocyte

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Cited by 5 publications
(6 citation statements)
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“…It mediates synoviocyte proliferation and is responsible for pain and inflammatory responses. PGE 2 enhances the degradative processes of proteoglycans 17,18 . It is found in diseased joints and is significantly elevated in synovial fluid of OA patients 15,18 .…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…It mediates synoviocyte proliferation and is responsible for pain and inflammatory responses. PGE 2 enhances the degradative processes of proteoglycans 17,18 . It is found in diseased joints and is significantly elevated in synovial fluid of OA patients 15,18 .…”
Section: Discussionmentioning
confidence: 99%
“…The synthesis of PGE 2 correlates with up-regulation of COX-2 and mPGEs1 6,16 . PGE 2 elicits its catabolic effect on articular cartilage by enhancing MMP production and proteoglycan degradation and by inhibiting synthesis of TIMPs 17,18 .…”
Section: Introductionmentioning
confidence: 99%
“…NSAIDs are most frequently used in OA and RA therapy and are shown to downregulate the production of MMPs from chondrocytes 26,27 . Therefore, the effects of NSAIDs (aspirin, diclofenac sodium, loxoprofen-SRS and NS398) on the release of m-calpain induced by 10 ng/ml TNF-a were further investigated.…”
Section: Nsaids Inhibited Tnf-a-induced M-calpain Releasementioning
confidence: 99%
“…In contrast, recent studies have reported that various NSAIDs have protective effects on the cartilage against arthritic damages 26e28 . For example, NSAIDs downregulated the production of MMP-1, -3, -9 and -13 from chondrocytes 26,27 . NSAIDs are also reported to protect chondrocytes from staurosporin-induced apoptotic death 28 .…”
Section: Introductionmentioning
confidence: 99%
“…However, this potential role needs to be clarified. PGE2 is also significantly elevated in the synovial fluid of OA patients 40 and it enhances the degradative process of proteoglycans in cartilage 41 . Thus, we can speculate that the inhibition of PGE2 production by CS could decrease bone sclerosis and could also have an anti-degradative effect in the deep zone of OA cartilage.…”
Section: Discussionmentioning
confidence: 99%