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

化学介质在腰椎椎间盘突出中的作用

基本信息

  • 批准号:
    08671658
  • 负责人:
  • 金额:
    $ 1.41万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    1996
  • 资助国家:
    日本
  • 起止时间:
    1996 至 1997
  • 项目状态:
    已结题

项目摘要

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.
最近有报道说,保守治疗期间,腰椎挤压盘材料的自发消退。 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在挤压盘材料的边缘和IL-1Alpha,beta,TNF-Alpha的边缘检测到软骨,刺激了圆盘材料中MMP-1,3和TIMP的产生。 MMP-3和TIMP的不平衡可能导致挤出盘材料的回归。ProstaglandinE_2(PGE_2)似乎在炎症过程中疼痛的发展中起着重要作用。据报道,环氧酶-2(COX-2)是这种前列腺素合成过程中的关键酶之一。从组织学上讲,COX-2不仅被定位在入侵椎间盘椎间盘的炎性细胞中,而且还位于椎间盘细胞中。该结果表明COX-2可能在腰椎间盘突出症的病理学中发挥作用。通过RT-PCR,COX-2 mRNA强烈表达IL-1BETA和TNFALPHA刺激的椎间盘细胞进行6H孵育,而在未刺激的细胞中很少检测到Cox-2 mRNA表达。这项研究的结果表明,腰椎盘中的细胞通过促炎细胞因子的刺激表达COX-2。因此,炎症刺激可能会诱导COX-2,这涉及腰椎椎间盘突出症的疼痛在病理生理上的疼痛。

项目成果

期刊论文数量(5)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
M.Doita, et al.: "Immunohistologic Study of the Ruptured Intervertebral Disc of the Lumbar Spine" SPINE. 21-2. 235-239 (1996)
M.Doita 等人:“腰椎椎间盘破裂的免疫组织学研究”SPINE。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
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)
Takako Kanaya:“腰椎间盘突出组织的免疫组织学研究 - 蛋白水解酶及其产生能力 -”日本文学会杂志 69(8)。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
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  • 通讯作者:
M.Doita, et al: "Immunohistologic Study of the Ruptured Intervertebral Disc of the Lumbar Spine" Spine. 21-2. 235-239 (1996)
M.Doita 等人:“腰椎椎间盘破裂的免疫组织学研究” 脊柱。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
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)
Takako Kanatani:“来自 burber spin 隔离盘的细胞中基质金属蛋白酶 (MMP-1,3) 和基质金属蛋白酶抑制剂 (TIMP) 的产生”ISSLS。
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
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DOITA Minoru其他文献

DOITA Minoru的其他文献

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{{ truncateString('DOITA Minoru', 18)}}的其他基金

Development of minimally invasive system for treatment of low back pain using therapeutic gene
利用治疗基因开发治疗腰痛的微创系统
  • 批准号:
    18300169
  • 财政年份:
    2006
  • 资助金额:
    $ 1.41万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)

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  • 批准号:
    15K10269
  • 财政年份:
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