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抗氧化剂 Glycitin 通过拮抗核髓细胞的炎症和氧化应激来防止椎间盘退变。

The antioxidant Glycitin protects against intervertebral disc degeneration through antagonizing inflammation and oxidative stress in nucleus pulposus cells.

机构信息

Department of Orthopaedic Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China.

Department of Radiology, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China.

出版信息

Aging (Albany NY). 2023 Nov 28;15(23):13693-13709. doi: 10.18632/aging.205251.

DOI:10.18632/aging.205251
PMID:38019477
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10756108/
Abstract

Intervertebral disc degeneration (IVDD) is a kind of typical degenerative disorder of the skeletal muscle system caused by many factors including aging, abnormal mechanical stress and inflammatory responses. Glycitin is a natural isoflavone extracted from legumes. Previous studies have found that it is anti-inflammatory and promotes wound repair. However, the role of Glycitin in IVDD has not been elucidated. In the present research, we were surprised that Glycitin antagonized the NF-κB pathway activity. In addition, we also found that Glycitin alleviated TNF-α-induced metabolic disorders, extracellular matrix degradation, oxidative stress, inflammation responses, and mitochondrial damage. Furthermore, in experimental study, we discovered Glycitin attenuated IVDD. The results revealed that Glycitin alleviated the degenerative phenotype of IVDD. According to this research, Glycitin has anti-inflammatory properties that might exert a protective function in IVDD, suggesting a prospective therapeutic approach for IVDD.

摘要

椎间盘退变(IVDD)是一种由多种因素引起的典型骨骼肌肉系统退行性疾病,包括衰老、异常机械应力和炎症反应。黄豆苷原为从豆类中提取的天然异黄酮。先前的研究发现它具有抗炎和促进伤口修复的作用。然而,黄豆苷元在 IVDD 中的作用尚未阐明。在本研究中,我们惊讶地发现黄豆苷元拮抗 NF-κB 通路活性。此外,我们还发现黄豆苷元减轻了 TNF-α诱导的代谢紊乱、细胞外基质降解、氧化应激、炎症反应和线粒体损伤。此外,在实验研究中,我们发现黄豆苷元减轻了 IVDD。结果表明,黄豆苷元减轻了 IVDD 的退行性表型。根据这项研究,黄豆苷元具有抗炎特性,可能对 IVDD 发挥保护作用,为 IVDD 的治疗提供了新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/0476affd13d3/aging-15-205251-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/8818a7de8ce3/aging-15-205251-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/9ae4c63b2ed8/aging-15-205251-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/0476affd13d3/aging-15-205251-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/d1c5b02e9fe1/aging-15-205251-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/44c04d73243e/aging-15-205251-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/fedff2dd243c/aging-15-205251-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/d0b91fe1ebb0/aging-15-205251-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/8818a7de8ce3/aging-15-205251-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/9ae4c63b2ed8/aging-15-205251-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a5d/10756108/0476affd13d3/aging-15-205251-g007.jpg

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