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Inhibition of neutrophil-mediated chondrocyte cytotoxicity by nitric oxide (NO) generated by articular chondrocytes.

Research Project

Project/Area Number 06671454
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Orthopaedic surgery
Research InstitutionKobe University

Principal Investigator

SAURA Ryuichi  Kobe University Hospital, Assistant., 医学部・附属病院, 助手 (10252769)

Co-Investigator(Kenkyū-buntansha) MIZUNO Kosaku  Kobe uNiversity School of Medicine, Professor., 医学部, 教授 (90030981)
FUJIOKA Hiroyuki  Kobe University Hospital, Assistant., 医学部・附属病院, 助手 (10252777)
Project Period (FY) 1994 – 1995
Project Status Completed (Fiscal Year 1995)
Budget Amount *help
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
KeywordsRheumatoid arthritis / Cartilage degradation / Chondrocyte / Polymorphonuclear leukocyte / Hydrogen peroxide / Nitric oxide / Cytokines
Research Abstract

Nitric oxide (NO) was identified as an active product of the oxidative cleavage of L-arginine. NO is generated by endothelial cells, macrophages and neutrophils and the higher concentration of nitrite, which is the stable endproduct of NO,is detected in the rheumatoid synovial fluid and serum. It is recently reported that NO inhibits neutrophil superoxide anion production and, in this way, associated with tissue degradation in inflammatory process. We have reported that articular chondrocytes were damaged by hydrogen peroxide generated by activated neutrophils. We have studied, in this investigation, the effect of NO on neutrophil-mediated chondrocyte cytotoxicity. Primary monolayr culture of chondrocytes was obtained from bovine articular cartilage by collagenase digestion and neutrophils were separated from healthy human doners. Chondrocyte cytotoxicity was measured by chromium-51 (^<51>Cr) release from the prelabeled chondrocytes in the presence of neutrophils. The concentration of NO was measured as nitrite concentration by Grisse reaction. Articular chondrocytes synthesized NO by the stimulation of interleukin (IL-1alpha) and TNF-alpha for 24h in a dose-dependent fashion. In the presence of 100 muM of L-arginine, 200 U/ml of IL-1alpha yielded the significant generation (P<0.01) of NO (2muM nitrite equivalent) from chondrocytes. Neutrophils increased ^<51>Cr-release from articular chondrocytes, and this chondrocyte cytotoxicity was significantly (p<0.05) reversed by addition of 100 muM of L-arginine in the neutrophil-chondrocyte co-cultures In contrast, D-arginine failed to inhibit the neutrophil mediated chondrocyte cytotoxicity. These result suggested that NO generated from articular chondrocytes have a protective effect against the oxidative stress in inflammatory cartilage.

Report

(3 results)
  • 1995 Annual Research Report   Final Research Report Summary
  • 1994 Annual Research Report
  • Research Products

    (10 results)

All Other

All Publications (10 results)

  • [Publications] 藤田郁夫: "多核白血球による軟骨障害に対する軟骨細胞障害に対する軟骨細胞由来のNitric Oxyolaの影響" リウマチ. 33. 639-639 (1993)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Ikuo Fijita: "Inhbition of Newtrophil-mechiated chendvocyte cytoroxicingry Nitric oxide Gcvervred by Anicular chvrdocyte : Anovel Protedies Maharisn of the Contilage Degradation." Orthopaedic Tvanscct : ans. 18. 502-502 (1994)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Ikuo Fuita: "Inhbition of Newtrophil-mechiated chendvocyte cytoroxicingry Nitric oxide Gcvervred by Anicular chvrdocyte : Anovel Protedies Maharisn of the Contilage Degradation." Arthvitis and Rheurvatisn. 36. S189-S189 (1993)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Fujita, I.et al.: "Inhibition of neutrophil-mediated chondrocyte cytotoxicity by nitric oxide generated by articular chondrocytes ; A novel protective mechanism of the cartilage degradation." Arthritis Rheum.36. S189 (1993)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] Fujita, I., et al.: "Inhibition of neutrophil-mediated chondrocyte cytotoxicity by nitric oxide generated by articular chondrocytes ; A novel protective mechanism of the cartilage degradation." Orthop.Trans.18. 502 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1995 Final Research Report Summary
  • [Publications] 藤田郁夫: "多核白血球による軟骨細胞障害に対する軟骨細胞障害に対する軟骨細胞由来のnitric Oxideの影響" リウマチ. 33. 639-639 (1993)

    • Related Report
      1995 Annual Research Report
  • [Publications] Ikuo Fujita: "Inhibition of Neutrophil-mediated Chondrocute Cytotoxicity by Nitric Oxide Generated by Articular Chordrocyte: Novel Protective Mechanism of the Cartilage Degradation." Ortho paedic Transactions. 18. 502-502 (1994)

    • Related Report
      1995 Annual Research Report
  • [Publications] Ikuo Fujita: "Inhibition of Neutrophil-mediated Chondrocute Cytotoxicity by Nitric Oxide Generated by Articular Chordrocyte: Novel Protective Mechanism of the Cartilage Degradation." Arthtitis and Rheumatism. 36. S189-S189 (1993)

    • Related Report
      1995 Annual Research Report
  • [Publications] Ikuo Fujita: "Inhibiton of Neutriphil-mediated Chondrosyte Cytocoxicity by Nitric Oxide Generated by Articular ChondrocYte;A Novel Protein Mechanism of the Cartilage Degractation." ORTHOPAEDIC TRANSACTIONS. 18. 502-502 (1994)

    • Related Report
      1994 Annual Research Report
  • [Publications] Ikuo Fujita: "Inhibiton of Neutrophil-Medeted chondrocyte Cytotoxicity by Nitric Oxide Generated from Artcular Chondroytes;A Novel Rofedine Mochanism of the Coatilage Degractation." Arthritis and Rheumatism.36. S189-S189 (1993)

    • Related Report
      1994 Annual Research Report

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Published: 1994-04-01   Modified: 2016-04-21  

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