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淫羊藿苷在椎间盘退变中的治疗机制:一项批判性叙述性综述。

Therapeutic mechanisms of icariin in intervertebral disc degeneration: A critical narrative review.

作者信息

Zhong LiLun, Xu ZhenWen, Peng YingJun, Li SongPeng, Liu An, Lin ZhiDong

机构信息

Huizhou Hospital of Guangzhou University of Chinese Medicine (Huizhou Hospital of Traditional Chinese Medicine), 516000, Huizhou, PR China.

Huizhou Huicheng Hospital of Traditional Chinese Medicine, 516000, Huizhou, PR China.

出版信息

Biochem Biophys Rep. 2025 May 15;42:102047. doi: 10.1016/j.bbrep.2025.102047. eCollection 2025 Jun.

DOI:10.1016/j.bbrep.2025.102047
PMID:40486496
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12144494/
Abstract

Intervertebral disc degeneration (IDD), a primary cause of low back pain, involves complex pathological mechanisms. Current research emphasizes identifying strategies to mitigate degenerative processes and enhance intrinsic disc repair. Emerging evidence highlights the therapeutic potential of icariin (ICA) in promoting disc repair and delaying IDD progression. ICA exerts its effects through multiple mechanisms, including anti-inflammatory actions, oxidative stress mitigation, modulation of bone and collagen metabolism, and inhibition of ferroptosis and pyroptosis. This review synthesizes current research on ICA's therapeutic applications in IDD management.

摘要

椎间盘退变(IDD)是腰痛的主要原因,涉及复杂的病理机制。目前的研究重点是确定减轻退变过程和增强椎间盘自身修复的策略。新出现的证据突出了淫羊藿苷(ICA)在促进椎间盘修复和延缓IDD进展方面的治疗潜力。ICA通过多种机制发挥作用,包括抗炎作用、减轻氧化应激、调节骨和胶原蛋白代谢以及抑制铁死亡和焦亡。本综述综合了目前关于ICA在IDD治疗应用方面的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c2/12144494/3caf21faf01d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c2/12144494/3caf21faf01d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c2/12144494/3caf21faf01d/gr1.jpg

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本文引用的文献

1
Icariin inhibits chondrocyte ferroptosis and alleviates osteoarthritis by enhancing the SLC7A11/GPX4 signaling.淫羊藿苷通过增强 SLC7A11/GPX4 信号通路抑制软骨细胞铁死亡,从而缓解骨关节炎。
Int Immunopharmacol. 2024 May 30;133:112010. doi: 10.1016/j.intimp.2024.112010. Epub 2024 Apr 17.
2
Application and development of hydrogel biomaterials for the treatment of intervertebral disc degeneration: a literature review.水凝胶生物材料在椎间盘退变治疗中的应用与进展:文献综述
Front Cell Dev Biol. 2023 Dec 7;11:1286223. doi: 10.3389/fcell.2023.1286223. eCollection 2023.
3
Recent advances in the repair of degenerative intervertebral disc for preclinical applications.
用于临床前应用的退行性椎间盘修复的最新进展。
Front Bioeng Biotechnol. 2023 Sep 22;11:1259731. doi: 10.3389/fbioe.2023.1259731. eCollection 2023.
4
The role of ferroptosis in intervertebral disc degeneration.铁死亡在椎间盘退变中的作用。
Front Cell Dev Biol. 2023 Jul 27;11:1219840. doi: 10.3389/fcell.2023.1219840. eCollection 2023.
5
Icariin Promotes Osteogenic Differentiation in a Cell Model with NF1 Gene Knockout by Activating the cAMP/PKA/CREB Pathway.淫羊藿苷通过激活 cAMP/PKA/CREB 通路促进 NF1 基因敲除细胞模型中的成骨分化。
Molecules. 2023 Jun 30;28(13):5128. doi: 10.3390/molecules28135128.
6
Mitochondrial DNA induces nucleus pulposus cell pyroptosis via the TLR9-NF-κB-NLRP3 axis.线粒体 DNA 通过 TLR9-NF-κB-NLRP3 轴诱导髓核细胞焦亡。
J Transl Med. 2023 Jun 15;21(1):389. doi: 10.1186/s12967-023-04266-5.
7
The deubiquitinase USP11 ameliorates intervertebral disc degeneration by regulating oxidative stress-induced ferroptosis via deubiquitinating and stabilizing Sirt3.去泛素化酶 USP11 通过去泛素化和稳定 Sirt3 调节氧化应激诱导的铁死亡来改善椎间盘退变。
Redox Biol. 2023 Jun;62:102707. doi: 10.1016/j.redox.2023.102707. Epub 2023 Apr 20.
8
Cellular senescence - Molecular mechanisms of intervertebral disc degeneration from an immune perspective.细胞衰老——从免疫角度看椎间盘退变的分子机制。
Biomed Pharmacother. 2023 Jun;162:114711. doi: 10.1016/j.biopha.2023.114711. Epub 2023 Apr 20.
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BACH1 promotes intervertebral disc degeneration by regulating HMOX1/GPX4 to mediate oxidative stress, ferroptosis, and lipid metabolism in nucleus pulposus cells.BACH1 通过调节 HMOX1/GPX4 介导核髓细胞氧化应激、铁死亡和脂质代谢来促进椎间盘退变。
J Gene Med. 2023 Jun;25(6):e3488. doi: 10.1002/jgm.3488. Epub 2023 Apr 2.
10
Ferroptosis: A potential target for the intervention of intervertebral disc degeneration.铁死亡:干预椎间盘退变的潜在靶点。
Front Endocrinol (Lausanne). 2022 Oct 20;13:1042060. doi: 10.3389/fendo.2022.1042060. eCollection 2022.