Galangin Promotes Tendon Repair Mediated by Tendon-Derived Stem Cells through Activating the TGF-/31/Smad3 Signaling Pathway

被引:0
|
作者
Deng, Xiongwei [1 ]
Li, Qiang [1 ]
Yuan, Haitao [1 ]
Hu, Hejun [1 ]
Fan, Shaoyong [1 ]
机构
[1] Nanchang Hongdu Hosp Tradit Chinese Med, Dept Foot & Ankle Surg, Nanchang 330038, Jiangxi, Peoples R China
关键词
galangin; tendon repair; tendon-derived stem cell; transforming growth factor beta 1 (TGF-beta 1); Smad3; tendon injury; EXTRACELLULAR-MATRIX; INJURY; TENDINOPATHY;
D O I
10.1248/cpb.c24-00117
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
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 /3 1 (TGF-/31) /3 1) and p-Smad3 to activate the TGF-/31/Smad /3 1/Smad 3 signaling pathway, while GLN mediated collagen deposition in TDSCs was reversed by LY3200882, a TGF-/3 /3 receptor inhibitor. The study concluded that GLN-mediated TDSCs enhanced tendon repair by activating the TGF-/31/Smad /3 1/Smad 3 signaling pathway, suggesting a novel therapeutic option in treating tendon repair.
引用
收藏
页码:669 / 675
页数:7
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