Galangin Promotes Tendon Repair Mediated by Tendon-Derived Stem Cells through Activating the TGF-β1/Smad3 Signaling Pathway
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)...
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| Veröffentlicht in: | Chemical & pharmaceutical bulletin 2024/07/13, Vol.72(7), pp.669-675 |
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| creator | Deng, Xiongwei Li, Qiang Yuan, Haitao Hu, Hejun Fan, Shaoyong |
| description | 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. |
| doi_str_mv | 10.1248/cpb.c24-00117 |
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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.</description><identifier>ISSN: 0009-2363</identifier><identifier>ISSN: 1347-5223</identifier><identifier>EISSN: 1347-5223</identifier><identifier>DOI: 10.1248/cpb.c24-00117</identifier><identifier>PMID: 39010213</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>Alizarin ; Alkaline phosphatase ; Animals ; Cells, Cultured ; Collagen ; Collagen (type I) ; Decorin ; Deposition ; Flavonoids ; Flavonoids - chemistry ; Flavonoids - pharmacology ; Flow cytometry ; galangin ; Gene expression ; Growth factors ; Molecular modelling ; Orthopedics ; Proteins ; Rats ; Rats, Sprague-Dawley ; Signal transduction ; Signal Transduction - drug effects ; Smad3 ; Smad3 protein ; Smad3 Protein - antagonists & inhibitors ; Smad3 Protein - metabolism ; Staining ; Stem cells ; Stem Cells - cytology ; Stem Cells - drug effects ; Stem Cells - metabolism ; Tendon Injuries - drug therapy ; Tendon Injuries - metabolism ; tendon injury ; tendon repair ; tendon-derived stem cell ; Tendons ; Tendons - cytology ; Tendons - drug effects ; Tendons - metabolism ; Transforming Growth Factor beta1 - metabolism ; transforming growth factor β1 (TGF-β1) ; Transforming growth factor-b ; Transforming growth factor-b1</subject><ispartof>Chemical and Pharmaceutical Bulletin, 2024/07/13, Vol.72(7), pp.669-675</ispartof><rights>2024 Author(s) This is an open access article distributed under the terms of Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/). Published by The Pharmaceutical Society of Japan</rights><rights>2024. This work is published under https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3053-4e7e945b0e5a991b2787d94de05ed7b1c11bbac62e4b9927803b8f08665fd22a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39010213$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deng, Xiongwei</creatorcontrib><creatorcontrib>Li, Qiang</creatorcontrib><creatorcontrib>Yuan, Haitao</creatorcontrib><creatorcontrib>Hu, Hejun</creatorcontrib><creatorcontrib>Fan, Shaoyong</creatorcontrib><title>Galangin Promotes Tendon Repair Mediated by Tendon-Derived Stem Cells through Activating the TGF-β1/Smad3 Signaling Pathway</title><title>Chemical & pharmaceutical bulletin</title><addtitle>Chem. Pharm. Bull.</addtitle><description>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.</description><subject>Alizarin</subject><subject>Alkaline phosphatase</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Decorin</subject><subject>Deposition</subject><subject>Flavonoids</subject><subject>Flavonoids - chemistry</subject><subject>Flavonoids - pharmacology</subject><subject>Flow cytometry</subject><subject>galangin</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Molecular modelling</subject><subject>Orthopedics</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Smad3</subject><subject>Smad3 protein</subject><subject>Smad3 Protein - antagonists & inhibitors</subject><subject>Smad3 Protein - metabolism</subject><subject>Staining</subject><subject>Stem cells</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - drug effects</subject><subject>Stem Cells - metabolism</subject><subject>Tendon Injuries - drug therapy</subject><subject>Tendon Injuries - metabolism</subject><subject>tendon injury</subject><subject>tendon repair</subject><subject>tendon-derived stem cell</subject><subject>Tendons</subject><subject>Tendons - cytology</subject><subject>Tendons - drug effects</subject><subject>Tendons - metabolism</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>transforming growth factor β1 (TGF-β1)</subject><subject>Transforming growth factor-b</subject><subject>Transforming growth factor-b1</subject><issn>0009-2363</issn><issn>1347-5223</issn><issn>1347-5223</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkV2LEzEUhoMobl299FYC3ngzuyfJzGRyuVS3Cisutl6HZOZ0mjIfNcmsFPxV_hB_k-m2VvDmHDjvw8uBh5DXDK4Yz6vremevap5nAIzJJ2TGRC6zgnPxlMwAQGVclOKCvAhhC8ALkOI5uRAKGHAmZuTnwnRmaN1A7_3YjxEDXeHQjAP9ijvjPP2MjTMRG2r3pyR7j949pMsyYk_n2HWBxo0fp3ZDb-roHkx0Q5tOSFeL2-z3L3a97E0j6NK1g-kO2b2Jmx9m_5I8W5su4KvTviTfbj-s5h-zuy-LT_Obu6wWUIgsR4kqLyxgYZRilstKNipvEApspGU1Y9aauuSYW6VSCsJWa6jKslg3nBtxSd4de3d-_D5hiLp3oU6PmwHHKWgBFeOK5UIk9O1_6HacfHr7QCkBAmSZJyo7UrUfQ_C41jvveuP3moE-aNFJi05a9KOWxL85tU62x-ZM__WQgPkR2IZoWjwDxkdXd_hYJ7mWh3Gu_ZdujNc4iD9PrqAg</recordid><startdate>20240713</startdate><enddate>20240713</enddate><creator>Deng, Xiongwei</creator><creator>Li, Qiang</creator><creator>Yuan, Haitao</creator><creator>Hu, Hejun</creator><creator>Fan, Shaoyong</creator><general>The Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20240713</creationdate><title>Galangin Promotes Tendon Repair Mediated by Tendon-Derived Stem Cells through Activating the TGF-β1/Smad3 Signaling Pathway</title><author>Deng, Xiongwei ; Li, Qiang ; Yuan, Haitao ; Hu, Hejun ; Fan, Shaoyong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3053-4e7e945b0e5a991b2787d94de05ed7b1c11bbac62e4b9927803b8f08665fd22a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Alizarin</topic><topic>Alkaline phosphatase</topic><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Decorin</topic><topic>Deposition</topic><topic>Flavonoids</topic><topic>Flavonoids - chemistry</topic><topic>Flavonoids - pharmacology</topic><topic>Flow cytometry</topic><topic>galangin</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Molecular modelling</topic><topic>Orthopedics</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Smad3</topic><topic>Smad3 protein</topic><topic>Smad3 Protein - antagonists & inhibitors</topic><topic>Smad3 Protein - metabolism</topic><topic>Staining</topic><topic>Stem cells</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - drug effects</topic><topic>Stem Cells - metabolism</topic><topic>Tendon Injuries - drug therapy</topic><topic>Tendon Injuries - metabolism</topic><topic>tendon injury</topic><topic>tendon repair</topic><topic>tendon-derived stem cell</topic><topic>Tendons</topic><topic>Tendons - cytology</topic><topic>Tendons - drug effects</topic><topic>Tendons - metabolism</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>transforming growth factor β1 (TGF-β1)</topic><topic>Transforming growth factor-b</topic><topic>Transforming growth factor-b1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Deng, Xiongwei</creatorcontrib><creatorcontrib>Li, Qiang</creatorcontrib><creatorcontrib>Yuan, Haitao</creatorcontrib><creatorcontrib>Hu, Hejun</creatorcontrib><creatorcontrib>Fan, Shaoyong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Chemical & pharmaceutical bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deng, Xiongwei</au><au>Li, Qiang</au><au>Yuan, Haitao</au><au>Hu, Hejun</au><au>Fan, Shaoyong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Galangin Promotes Tendon Repair Mediated by Tendon-Derived Stem Cells through Activating the TGF-β1/Smad3 Signaling Pathway</atitle><jtitle>Chemical & pharmaceutical bulletin</jtitle><addtitle>Chem. Pharm. Bull.</addtitle><date>2024-07-13</date><risdate>2024</risdate><volume>72</volume><issue>7</issue><spage>669</spage><epage>675</epage><pages>669-675</pages><artnum>c24-00117</artnum><issn>0009-2363</issn><issn>1347-5223</issn><eissn>1347-5223</eissn><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.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>39010213</pmid><doi>10.1248/cpb.c24-00117</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Alizarin Alkaline phosphatase Animals Cells, Cultured Collagen Collagen (type I) Decorin Deposition Flavonoids Flavonoids - chemistry Flavonoids - pharmacology Flow cytometry galangin Gene expression Growth factors Molecular modelling Orthopedics Proteins Rats Rats, Sprague-Dawley Signal transduction Signal Transduction - drug effects Smad3 Smad3 protein Smad3 Protein - antagonists & inhibitors Smad3 Protein - metabolism Staining Stem cells Stem Cells - cytology Stem Cells - drug effects Stem Cells - metabolism Tendon Injuries - drug therapy Tendon Injuries - metabolism tendon injury tendon repair tendon-derived stem cell Tendons Tendons - cytology Tendons - drug effects Tendons - metabolism Transforming Growth Factor beta1 - metabolism transforming growth factor β1 (TGF-β1) Transforming growth factor-b Transforming growth factor-b1 |
| title | Galangin Promotes Tendon Repair Mediated by Tendon-Derived Stem Cells through Activating the TGF-β1/Smad3 Signaling Pathway |
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