Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of several nonsteroidal antiinflammatory drugs, used at concentrations achievable in synovial fluid, on human osteoarthritic (OA) cartilage metallo-protease activity in vitro was studied. Acetaminophen and ketoprofen had no effect; sodium salicylate, indomethacin, and diclofenac slightly decreased proteoglycanase activity. Piroxicam and tenoxicam suppressed proteoglycanase activity by 48.2% and 68.3%, respectively, and suppressed collagenase activity by 19.1% and 36.8%, respectively. Use of these NSAIDs may help to decrease cartilage catabolism in patients with OA.
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PMID:In vitro effect of nonsteroidal antiinflammatory drugs on proteoglycanase and collagenase activity in human osteoarthritic cartilage. 165 6

To assess the effects of heparin on bone formation we measured [3H]proline incorporation into collagenase-digestible (CDP) and noncollagen protein (NCP), [3H]thymidine (TdR) incorporation into DNA, and DNA content in 21-day-old fetal rat calvaria cultured in BGJ medium with bovine serum albumin for 24-96 hours. Heparin at 5-125 micrograms/ml decreased TdR incorporation by 26-51% at 24 and 96 hours. At 96 hours, heparin 5, 25, and 125 micrograms/ml decreased [3H]proline incorporation into CDP by 41, 48, and 32%, respectively, with no significant change in NCP. To evaluate the possible role of PGE2 in these inhibitory responses, media PGE2 concentration was measured and the effects of heparin on CDP labeling and DNA synthesis were tested in the presence of indomethacin, piroxicam, and flurbiprofen to inhibit endogenous prostaglandin E2 (PGE2) production and in the presence of a high concentration (10(-7) M) of exogenous PGE2. Heparin did not alter PGE2 production at 24 hours but at 48 hours there was a significant reduction. At 96 hours, indomethacin (10(-6) M) inhibited [3H]-proline incorporation into CDP by 38% but had no effect on the labeling of NCP. Heparin had no further significant inhibitory effect in the presence of indomethacin. Piroxicam and flurbiprofen did not alter DNA content and had a smaller inhibitory effect than indomethacin on the labeling of CDP. Moreover, addition of heparin produced a further inhibition of CDP and DNA content and finally, heparin decreased CDP labeling by 71% in the presence of PGE2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of heparin on bone formation in cultured fetal rat calvaria. 210 77

Piroxicam and other antiarthritic drugs were compared with respect to their effects on T-lymphocyte/monocyte/rheumatoid synovial cell interactions leading to inflammatory mediator production. Piroxicam inhibited PGE2 formation by blood mononuclear cells, but was less potent than indomethacin. Both drugs enhanced suboptimal phytohemagglutinin (PHA)-stimulated tritiated thymidine (3H-TdR) incorporation by mononuclear cells, although optimal responses were less affected. Exogenous interleukin-2 (IL-2) enhanced suboptimal but not optimal PHA responses, and the effects of the cyclo-oxygenase inhibitors were overcome by exogenous PGE2. Thus piroxicam and indomethacin prevented the inhibition by endogenous monocyte-derived PGE2 of IL-2 secretion and activity. Other antiarthritic drugs, including antimalarials, immunosuppressive agents and gold salts, inhibited PHA-induced lymphocyte proliferation regardless of the level of stimulation. Mepacrine and chloroquine were more effective in inhibiting the release of mononuclear cell factor (MCF) that stimulated PGE2 synthesis by synovial cells. Cyclosporin-A, azathioprine and 6-mercaptopurine were more potent as antiproliferative agents than as inhibitors of mediator release. Sodium aurothiomalate and aurothioglucose selectively interfered with lymphocyte-mediated amplification of MCF release, whereas auranofin inhibited spontaneous production of monocytes and the action of MCF on synovial cells. In rheumatoid synovial cells, piroxicam and indomethacin inhibited PGE2 production but not collagenase release. Suppression of MCF release could lead indirectly to reduction of IL-2 and collagenase as well as PGE2 production and consequently to more profound inhibition of immunologically-mediated inflammation.
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PMID:Effects of piroxicam on mononuclear cells. Comparison with other antiarthritic drugs. 633 79