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褪黑素在椎间盘退变治疗中的研究进展

Progress of melatonin in the treatment of intervertebral disc degeneration.

作者信息

Yin Jianlin, Wan Lei, Zhang Kuaixiang, Yang Jiangjia, Liu Man, Zhao Mingyu, Li Jitian

机构信息

Henan University of Chinese Medicine, Henan Luoyang Orthopedic Hospital (Henan Provincial Orthopedic Hospital), Zhengzhou, China.

Department of Osteology, The Second Affiliated Hospital of Luohe Medical College, Luohe, China.

出版信息

Front Physiol. 2025 May 14;16:1529315. doi: 10.3389/fphys.2025.1529315. eCollection 2025.

Abstract

The most common degenerative condition affecting the musculoskeletal system, and the leading cause of persistent low back pain, is intervertebral disc degeneration (IDD). IDD is increasingly common with age and has a variety of etiologic factors including inflammation, oxidative stress, extracellular matrix (ECM) degradation, and apoptosis that interact with each other to cause IDD. Because it is difficult to determine the exact pathogenesis of IDD, there is a lack of effective therapeutic agents. Melatonin has been intensively studied for its strong anti-inflammatory, antioxidant, and anti-apoptotic properties. Melatonin is a pleiotropic indole-stimulating hormone produced by the pineal gland, which can be used to treat a wide range of degenerative diseases. Therefore, melatonin supplementation may be a viable treatment for IDD. This article reviews the current mechanisms of IDD and the multiple roles regarding melatonin's anti-inflammatory, antioxidant, anti-apoptotic, and mitigating ECM degradation in IDD, incorporating new current research perspectives, as well as recent studies on drug delivery systems.

摘要

影响肌肉骨骼系统最常见的退行性疾病,也是持续性腰痛的主要原因,是椎间盘退变(IDD)。IDD随着年龄增长越来越常见,有多种病因,包括炎症、氧化应激、细胞外基质(ECM)降解和细胞凋亡,这些因素相互作用导致IDD。由于难以确定IDD的确切发病机制,缺乏有效的治疗药物。褪黑素因其强大的抗炎、抗氧化和抗凋亡特性而受到深入研究。褪黑素是松果体分泌的一种具有多种功能的吲哚刺激激素,可用于治疗多种退行性疾病。因此,补充褪黑素可能是治疗IDD的一种可行方法。本文综述了IDD的当前发病机制,以及褪黑素在IDD中的抗炎、抗氧化、抗凋亡和减轻ECM降解的多种作用,纳入了新的当前研究观点以及药物递送系统的最新研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6104/12116318/1757ebcdfbbf/fphys-16-1529315-g001.jpg

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