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The role of chemical mediators in the extruded intervertebral disc of lumbar spine

Research Project

Project/Area Number 08671658
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Orthopaedic surgery
Research InstitutionKobe University

Principal Investigator

DOITA Minoru  Kobe University, School of Medicine, Assistant Professor, 医学部, 助手 (60237170)

Co-Investigator(Kenkyū-buntansha) HARADA Toshihiko  Kobe University, School of Medicine, Lecturer, 医学部, 講師 (80228650)
Project Period (FY) 1996 – 1997
Project Status Completed (Fiscal Year 1997)
Budget Amount *help
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
Keywordslumbar disc herniation / basic FGF / immunohistochemical study / Matrix metalloproteinase-1,3 / Interleukin-1 / cyclooxygenase-2 / matrix metalloproteinases / immunohistological study
Research Abstract

It has been recently reported that the spontaneous regression of the extruded disc materials of lumbar spine during the conservative treatment. The chemical mesiators released from those inflammatory cells, which are usually observed at the edge of extruded disc materials, may play important roles in producing matrix metalloproteases which in turn will change pain or regression of extruded disc materials.
It is revealed that IL-1alpha, beta, TNF-alpha, matrix metalloproteases-1 and 3 (MMP-1,3) which play important roles in destroyin of the articular cartilage were detected in the at the edge of the extruded disc materials and IL-1alpha, beta, TNF-alpha stimulate the production of MMP-1,3 and TIMP in the disc materials. The inbalance of MMP-3 and TIMP may lead to the regression of the extruded disc materials.
Prostaglandin E_2 (PGE_2) seems to play an important role in the development of the pain in inflammatory process. Cyclooxgenase-2 (COX-2) is reported to be one of the key enzymes in the process of this prostagladin synthesis. Histologically, COX-2 was localized not only in the inflammatory cells invaded into the herniated disc but also in the disc cells. This result indicates that COX-2 may play a role in the pathology of the lumbar disc herniation. By the RT-PCR,COX-2 mRNA was strongly expressed both IL-1beta and TNFalpha-stimulated disc cells for 6h incubation, while little COX-2 mRNA expression was detected in unstimulated cells. The results in this study reveal that the cells in the lumbar disc express COX-2 by the stimulation of the proinflammatory cytokines. It is, therefore, suggested that inflammatory stimulation might induce COX-2, which concerns to the pain induction of lumbar disc herniation pathophysiologically.

Report

(3 results)
  • 1997 Annual Research Report   Final Research Report Summary
  • 1996 Annual Research Report
  • Research Products

    (5 results)

All Other

All Publications (5 results)

  • [Publications] M.Doita, et al.: "Immunohistologic Study of the Ruptured Intervertebral Disc of the Lumbar Spine" SPINE. 21-2. 235-239 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] M.Doita, et al.: "Immunohistologic Study of the Ruptured Intervertebral Disc of the Lumbar Spine" SPINE. 21-2. 235-239 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] M.Doita, et al: "Immunohistologic Study of the Ruptured Intervertebral Disc of the Lumbar Spine" Spine. 21-2. 235-239 (1996)

    • Related Report
      1997 Annual Research Report
  • [Publications] 金谷 貴子: "腰椎々間板ヘルニア組織の免疫組織学的検討-蛋白分解酵素とその産生能-" 日整会誌. 69(8). S1452- (1995)

    • Related Report
      1996 Annual Research Report
  • [Publications] Takako Kanatani: "The production of matrix metalloproterhasis (MMP-1,3) and the inhibitor of matrix metalloproterinase (TIMP) in the cells from sequestrated disc of burber spin" ISSLS. June. (1996)

    • Related Report
      1996 Annual Research Report

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Published: 1996-04-01   Modified: 2016-04-21  

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