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腰椎间盘突出症会自发产生基质金属蛋白酶、一氧化氮、白细胞介素-6和前列腺素E2。

Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2.

作者信息

Kang J D, Georgescu H I, McIntyre-Larkin L, Stefanovic-Racic M, Donaldson W F, Evans C H

机构信息

Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pennsylvania, USA.

出版信息

Spine (Phila Pa 1976). 1996 Feb 1;21(3):271-7. doi: 10.1097/00007632-199602010-00003.

Abstract

STUDY DESIGN

Herniated lumbar disc specimens were obtained from patients undergoing surgical discectomy for persistent radiculopathy and cultured in vitro to determine whether various biochemical agents were being produced.

OBJECTIVES

Our hypothesis is that biochemical mediators of inflammation and tissue degradation play a role in intervertebral disc degeneration and in the pathophysiology of radiculopathy.

SUMMARY OF BACKGROUND DATA

Low back pain with or without radiculopathy is a significant clinical problem, but the etiology of low back pain and the exact pathophysiology of radiculopathy remain elusive. The biochemical events that occur with intervertebral disc degeneration and, in particular, the role of biochemical mediators of inflammation and tissue degradation have received sparse attention in the literature. There is some preliminary evidence that inflammatory mediators may have an important role in the pathophysiology of radiculopathy.

METHODS

Eighteen herniated lumbar discs were obtained from 15 patients undergoing disc surgery. The specimens were cultured and incubated for 72 hours, and the media were collected subsequently for biochemical analysis. Biochemical assays for matrix metalloproteinases, nitric oxide, prostaglandin E2, and a variety of cytokines were performed. As a control group, eight lumbar disc specimens were obtained from four patients undergoing anterior surgery for scoliosis and traumatic burst fractures, and similar biochemical analyses were performed.

RESULTS

The culture media from the herniated lumbar discs showed increased levels of matrix metalloproteinase activity compared with the control discs. Similarly, the levels of nitric oxide, prostaglandin E2, and interleukin-6 were significantly higher in the herniated discs compared with the control discs. Interleukin 1 alpha, interleukin-1 beta, tumor necrosis factor-alpha, interleukin-1 receptor antagonist protein, and substance P were not detected in the culture media of either the herniated or control discs.

CONCLUSIONS

Herniated lumbar discs were making spontaneously increased amounts of matrix metalloproteinases, nitric oxide, prostaglandin E2, and interleukin-6. These products may be involved intimately in the biochemistry of disc degeneration and the pathophysiology of radiculopathy. Their exact roles certainly need further investigation, but their mere presence implicates biochemical processes in intervertebral disc degeneration.

摘要

研究设计

从因持续性神经根病接受手术椎间盘切除术的患者获取腰椎间盘突出标本,并在体外培养以确定是否产生了各种生化因子。

目的

我们的假设是炎症和组织降解的生化介质在椎间盘退变和神经根病的病理生理学中起作用。

背景数据总结

伴有或不伴有神经根病的下腰痛是一个重要的临床问题,但下腰痛的病因和神经根病的确切病理生理学仍不清楚。椎间盘退变时发生的生化事件,尤其是炎症和组织降解的生化介质的作用,在文献中受到的关注较少。有一些初步证据表明炎症介质可能在神经根病的病理生理学中起重要作用。

方法

从15例接受椎间盘手术的患者获取18个腰椎间盘突出标本。将标本培养并孵育72小时,随后收集培养基进行生化分析。进行基质金属蛋白酶、一氧化氮、前列腺素E2和多种细胞因子的生化检测。作为对照组,从4例因脊柱侧弯和创伤性爆裂骨折接受前路手术的患者获取8个腰椎间盘标本,并进行类似的生化分析。

结果

与对照椎间盘相比,腰椎间盘突出标本的培养基显示基质金属蛋白酶活性水平升高。同样,与对照椎间盘相比,腰椎间盘突出标本中一氧化氮、前列腺素E2和白细胞介素-6的水平显著更高。在腰椎间盘突出或对照标本的培养基中均未检测到白细胞介素1α、白细胞介素-1β、肿瘤坏死因子-α、白细胞介素-1受体拮抗剂蛋白和P物质。

结论

腰椎间盘突出标本自发产生的基质金属蛋白酶、一氧化氮、前列腺素E2和白细胞介素-6的量增加。这些产物可能密切参与椎间盘退变的生物化学过程和神经根病的病理生理学。它们的确切作用肯定需要进一步研究,但它们的存在表明椎间盘退变中存在生化过程。

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