Galangin Promotes Tendon Repair Mediated by Tendon-Derived Stem Cells through Activating the TGF-β1/Smad3 Signaling Pathway

IF 1.5 4区医学 Q4 CHEMISTRY, MEDICINAL Chemical & pharmaceutical bulletin Pub Date : 2024-07-13 DOI:10.1248/cpb.c24-00117

Xiongwei Deng, Qiang Li, Haitao Yuan, Hejun Hu, Shaoyong Fan

{"title":"Galangin Promotes Tendon Repair Mediated by Tendon-Derived Stem Cells through Activating the TGF-β1/Smad3 Signaling Pathway","authors":"Xiongwei Deng, Qiang Li, Haitao Yuan, Hejun Hu, Shaoyong Fan","doi":"10.1248/cpb.c24-00117","DOIUrl":null,"url":null,"abstract":"Tendon injury is a prevalent orthopedic disease that currently lacks effective treatment. Galangin (GLN) is a vital flavonoid found abundantly in galangal and is known for its natural activity. This study aimed to investigate the GLN-mediated molecular mechanism of tendon-derived stem cells (TDSCs) in tendon repair. The TDSCs were characterized using alkaline phosphatase staining, alizarin red S staining, oil red O staining, and flow cytometry. The effect of GLN treatment on collagen deposition was evaluated using Sirius red staining and quantitative (q)PCR, while a Western bot was used to assess protein levels and analyze pathways. Results showed that GLN treatment not only increased the collagen deposition but also elevated the mRNA expression and protein levels of multiple tendon markers like collagen type I alpha 1 (COL1A1), decorin (DCN) and tenomodulin (TNMD) in TDSCs. Moreover, GLN was also found to upregulate the protein levels of transforming growth factor β1 (TGF-β1) and p-Smad3 to activate the TGF-β1/Smad3 signaling pathway, while GLN mediated collagen deposition in TDSCs was reversed by LY3200882, a TGF-β receptor inhibitor. The study concluded that GLN-mediated TDSCs enhanced tendon repair by activating the TGF-β1/Smad3 signaling pathway, suggesting a novel therapeutic option in treating tendon repair.\n\n<img alt=\"\" src=\"https://www.jstage.jst.go.jp/pub/cpb/72/7/72_c24-00117/figure/72_c24-00117.png\"/>\nFullsize Image","PeriodicalId":9773,"journal":{"name":"Chemical & pharmaceutical bulletin","volume":null,"pages":null},"PeriodicalIF":1.5000,"publicationDate":"2024-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Chemical & pharmaceutical bulletin","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1248/cpb.c24-00117","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CHEMISTRY, MEDICINAL","Score":null,"Total":0}

引用次数: 0

Abstract

Tendon injury is a prevalent orthopedic disease that currently lacks effective treatment. Galangin (GLN) is a vital flavonoid found abundantly in galangal and is known for its natural activity. This study aimed to investigate the GLN-mediated molecular mechanism of tendon-derived stem cells (TDSCs) in tendon repair. The TDSCs were characterized using alkaline phosphatase staining, alizarin red S staining, oil red O staining, and flow cytometry. The effect of GLN treatment on collagen deposition was evaluated using Sirius red staining and quantitative (q)PCR, while a Western bot was used to assess protein levels and analyze pathways. Results showed that GLN treatment not only increased the collagen deposition but also elevated the mRNA expression and protein levels of multiple tendon markers like collagen type I alpha 1 (COL1A1), decorin (DCN) and tenomodulin (TNMD) in TDSCs. Moreover, GLN was also found to upregulate the protein levels of transforming growth factor β1 (TGF-β1) and p-Smad3 to activate the TGF-β1/Smad3 signaling pathway, while GLN mediated collagen deposition in TDSCs was reversed by LY3200882, a TGF-β receptor inhibitor. The study concluded that GLN-mediated TDSCs enhanced tendon repair by activating the TGF-β1/Smad3 signaling pathway, suggesting a novel therapeutic option in treating tendon repair.

Fullsize Image

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

高良姜素通过激活 TGF-β1/Smad3 信号通路促进肌腱衍生干细胞介导的肌腱修复

肌腱损伤是一种常见的骨科疾病，目前缺乏有效的治疗方法。高良姜素（GLN）是一种重要的黄酮类化合物，大量存在于高良姜中，以其天然活性而闻名。本研究旨在探讨GLN介导的肌腱衍生干细胞（TDSCs）修复肌腱的分子机制。研究人员使用碱性磷酸酶染色法、茜素红 S 染色法、油红 O 染色法和流式细胞仪对 TDSCs 进行了表征。使用天狼星红染色和定量（q）PCR评估了GLN处理对胶原沉积的影响，并使用Western bot评估蛋白质水平和分析通路。结果表明，GLN 处理不仅增加了胶原沉积，还提高了 TDSCs 中多种肌腱标记物的 mRNA 表达和蛋白水平，如Ⅰ型胶原α1（COL1A1）、decorin（DCN）和 tenomodulin（TNMD）。此外，研究还发现 GLN 能上调转化生长因子 β1（TGF-β1）和 p-Smad3 的蛋白水平，从而激活 TGF-β1/Smad3 信号通路，而 TGF-β 受体抑制剂 LY3200882 能逆转 GLN 介导的 TDSCs 胶原沉积。研究得出结论：GLN介导的TDSCs通过激活TGF-β1/Smad3信号通路增强了肌腱修复，为治疗肌腱修复提供了一种新的治疗方案。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Chemical & pharmaceutical bulletin 医学-化学综合

CiteScore

3.20

自引率

5.90%

发文量

132

审稿时长

1.7 months

期刊介绍： The CPB covers various chemical topics in the pharmaceutical and health sciences fields dealing with biologically active compounds, natural products, and medicines, while BPB deals with a wide range of biological topics in the pharmaceutical and health sciences fields including scientific research from basic to clinical studies. For details of their respective scopes, please refer to the submission topic categories below. Topics: Organic chemistry In silico science Inorganic chemistry Pharmacognosy Health statistics Forensic science Biochemistry Pharmacology Pharmaceutical care and science Medicinal chemistry Analytical chemistry Physical pharmacy Natural product chemistry Toxicology Environmental science Molecular and cellular biology Biopharmacy and pharmacokinetics Pharmaceutical education Chemical biology Physical chemistry Pharmaceutical engineering Epidemiology Hygiene Regulatory science Immunology and microbiology Clinical pharmacy Miscellaneous.