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基于分子对接技术验证6-姜酚通过USP49抑制软骨退行性改变

杨澜波 苏春霞 赵晓非 杨艳梅 成彦 黄涛 王海彬

广东医学2024,Vol.45Issue(8):970-975,6.
广东医学2024,Vol.45Issue(8):970-975,6.DOI:10.13820/j.cnki.gdyx.20225221

基于分子对接技术验证6-姜酚通过USP49抑制软骨退行性改变

Validation of 6-Gingerol in inhibiting cartilage degeneration through USP49 via molecular docking technology

杨澜波 1苏春霞 1赵晓非 1杨艳梅 1成彦 1黄涛 2王海彬3

作者信息

  • 1. 河南省洛阳正骨医院(河南省骨科医院)运动医学中心(河南洛阳 471002)
  • 2. 联勤保障部队第989医院骨科(河南洛阳 471031)
  • 3. 广州中医药大学第一附属医院骨科(广东广州 510405)
  • 折叠

摘要

Abstract

Objective To understand the effects and underlying mechanisms of 6-gingerol on chondrocyte apop-tosis and cartilage degradation in osteoarthritis.Methods The active components of traditional Chinese medicine that sig-nificantly upregulate USP49 expression(6-gingerol)were screened and subjected to molecular docking.Subsequently,IL-1 β-induced chondrocytes were treated with different concentrations of 6-gingerol,and the apoptosis of chondrocytes and the expression of USP49,β-catenin,and cartilage degradation-related proteins(MMP-1,MMP-13)were de-tected.Results The screening revealed that 6-gingerol significantly promotes the expression of USP49.Molecular doc-king showed a high-efficiency binding between 6-gingerol and USP49.After treating IL-1β-induced chondrocytes with different concentrations of 6-gingerol,the expression of USP49 was significantly upregulated,and the apoptosis of chondrocytes and the expression of β-catenin,MMP-1,and MMP-13 were inhibited.Conclusion 6-gingerol regu-lates the Wnt/β-catenin signaling pathway by upregulating USP49 expression,inhibits chondrocyte apoptosis and the ex-pression of cartilage degradation-related proteins MMP-1 and MMP-13,thereby alleviating IL-1 β-induced cartilage degeneration.

关键词

6-姜酚/泛素特异性蛋白酶-49/分子对接/Wnt/β-catenin通路

Key words

6-gingerol/Ubiquitin specific proteases 49/Molecular docking/Wnt/β-catenin pathway

分类

医药卫生

引用本文复制引用

杨澜波,苏春霞,赵晓非,杨艳梅,成彦,黄涛,王海彬..基于分子对接技术验证6-姜酚通过USP49抑制软骨退行性改变[J].广东医学,2024,45(8):970-975,6.

基金项目

河南省中医药科学研究专项基金资助项目(20-21ZY2230) (20-21ZY2230)

广东医学

OACSTPCD

1001-9448

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