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白细胞介素-1β和肿瘤坏死因子-α在椎间盘退变中的作用。

The role of IL-1β and TNF-α in intervertebral disc degeneration.

机构信息

Department of Spinal Surgery, The First Hospital of Jilin University, Changchun, 130021, China.

Department of Spinal Surgery, The First Hospital of Jilin University, Changchun, 130021, China.

出版信息

Biomed Pharmacother. 2020 Nov;131:110660. doi: 10.1016/j.biopha.2020.110660. Epub 2020 Aug 24.

DOI:10.1016/j.biopha.2020.110660
PMID:32853910
Abstract

Low back pain (LBP), a prevalent and costly disease around the world, is predominantly caused by intervertebral disc (IVD) degeneration (IDD). LBP also presents a substantial burden to public health and the economy. IDD is mainly caused by aging, trauma, genetic susceptibility, and other factors. It is closely associated with changes in tissue structure and function, including progressive destruction of the extracellular matrix (ECM), enhanced senescence, disc cell death, and impairment of tissue biomechanical function. The inflammatory process, exacerbated by cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), are considered to be the key mediators of IDD and LBP. IL-1β and TNF-α are the most important proinflammatory cytokines, as they have powerful proinflammatory activities and can promote the secretion of a variety of proinflammatory mediators. They are also upregulated in the degenerative IVDs, and they are closely related to various pathological IDD processes, including inflammatory response, matrix destruction, cellular senescence, autophagy, apoptosis, pyroptosis, and proliferation. Therefore, anti-IL-1β and anti-TNF-α therapies may have the potential to alleviate disc degeneration and LBP. In this paper, we reviewed the expression pattern and signal transduction pathways of IL-1β and TNF-α, and we primarily focused on their similar and different roles in IDD. Because IL-1β and TNF-α inhibition have the potential to alleviate IDD, an in-depth understanding of the role of IL-1β and TNF-α in IDD will benefit the development of new treatment methods for disc degeneration with IL-1β and TNF-α at the core.

摘要

下背痛(LBP)是一种在全球范围内普遍存在且代价高昂的疾病,主要由椎间盘(IVD)退变(IDD)引起。LBP 也给公共卫生和经济带来了巨大负担。IDD 主要由衰老、创伤、遗传易感性等因素引起。它与组织结构和功能的变化密切相关,包括细胞外基质(ECM)的渐进性破坏、衰老增强、椎间盘细胞死亡以及组织生物力学功能受损。炎症过程,加剧细胞因子白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α),被认为是 IDD 和 LBP 的关键介质。IL-1β 和 TNF-α 是最重要的促炎细胞因子,因为它们具有强大的促炎活性,可以促进多种促炎介质的分泌。它们在退变的 IVD 中也上调,与各种病理 IDD 过程密切相关,包括炎症反应、基质破坏、细胞衰老、自噬、细胞凋亡、细胞焦亡和增殖。因此,抗 IL-1β 和抗 TNF-α 治疗可能有潜力缓解椎间盘退变和 LBP。本文综述了 IL-1β 和 TNF-α 的表达模式和信号转导途径,主要关注它们在 IDD 中的相似和不同作用。由于 IL-1β 和 TNF-α 抑制有潜力缓解 IDD,深入了解 IL-1β 和 TNF-α 在 IDD 中的作用将有助于开发以 IL-1β 和 TNF-α 为核心的椎间盘退变的新治疗方法。

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