Inhibition of interleukin 1-beta induced rat and human cartilage degradation in vitro by the metalloproteinase inhibitor U27391
Article Abstract:
The metalloproteinase inhibitor U27391 may slow the cartilage breakdown induced by interleukin 1 (IL-1) in patients suffering from disorders such as osteoarthritis or rheumatoid arthritis. Osteoarthritis and rheumatoid arthritis are inflammatory disorders that affect the joints. A study examined the effect of metalloproteinase inhibitor U27391 on the degradation of rat or human cartilage induced by recombinant (genetically engineered) IL-1-beta. Different concentrations of U27391 decreased IL-1-induced cartilage loss in both rats and humans. U27391 also lessened the blocking of cartilage synthesis in both rat and human cartilage. Increased levels of IL-1 are present at sites of inflammation in patients suffering from osteoarthritis or rheumatoid arthritis. IL-1 may induce the release of metalloproteinases, a group of enzymes that are capable of degrading cartilage.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1993
User Contributions:
Comment about this article or add new information about this topic:
Effect of tenidap on cartilage integrity in vitro
Article Abstract:
Treatment with the drug tenidap may reduce cartilage degradation in patients with rheumatoid arthritis (RA). The drug may act by blocking the adverse effect of cytokines such as interleukin 1 (IL-1) on cartilage metabolism. A study examined the effect of human recombinant (genetically engineered) IL-1-alpha and different non-steroidal anti-inflammatory drugs (NSAIDs) on cartilage metabolism in animal tissue. IL-1-alpha increased cartilage degradation and interfered with cartilage synthesis. Tenidap blocked the adverse effect of IL-1-alpha on cartilage degradation and to a lesser degree on cartilage synthesis. The NSAIDs diclofenac and naproxen did not block the adverse effect of IL-1-alpha on cartilage metabolism. Tenidap also increased cartilage repair during recovery from treatment with IL-1-alpha.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1993
User Contributions:
Comment about this article or add new information about this topic:
Influence of interleukin 1 beta on tenascin distribution in human normal and osteoarthritis cartilage: a quantitative immunohistochemical study
Article Abstract:
Interleukin-1 beta (IL-1beta) appears to increase the levels of tenascin in both normal and diseased cartilage tissues. Tenascin is a protein important to new tissue growth. Tenascin levels were measured after exposure to IL-1beta in normal cartilage samples and cartilage from patients with osteoarthritis. Similar samples not exposed to IL-1beta served as controls. IL-1beta exposure increased the overall tenascin levels in normal cartilage and in the outer layers of the diseased samples. Tenascin levels were higher in diseased control samples compared to the normal control samples.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1996
User Contributions:
Comment about this article or add new information about this topic:
- Abstracts: Endotoxin-induced fetal growth retardation in the pregnant guinea pig. Tumor necrosis factor-alpha in response to endotoxin administration in the pregnant guinea pig
- Abstracts: Intermittent sinusoidal heart rate pattern in vagotomized fetal lambs. Fetal heart rate patterns in postasphyxiated fetal lambs with brain damage
- Abstracts: Coalition presses to preserve affirmative action in medicine. Ready or not, here are outcomes 'report cards.' (outcomes research)
- Abstracts: AMA leaders renew push for Medicare overhaul plan. GOP health plan blitz: House plan gets tentative AMA nod; spending curbs a concern
- Abstracts: Medicaid proposal may cut physicians' pay; AMA fighting change on 'dual-eligibles.' (elderly persons qualified for both Medicare, Medicaid)