Yao Zhu, Chengyu Lin, Xudong Zhang, Zuyun Qiu, Lei Shi, Jianmin Li
{"title":"Mechanism of Astragaloside IV in Promoting Osteogenic Differentiation.","authors":"Yao Zhu, Chengyu Lin, Xudong Zhang, Zuyun Qiu, Lei Shi, Jianmin Li","doi":"10.2174/0115665240333454241203050356","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>This study focuses on exploring the impact of Astragaloside IV [AS-IV] on osteogenic differentiation.</p><p><strong>Methods: </strong>Osteogenic differentiation was induced in rat osteoblasts, following which treatment with AS-IV at varied doses was performed. Using Alizarin red staining and alkaline phosphatase [ALP] detection assay, the osteogenic differentiation of the cells was investigated. The expressions of osteogenic differentiation-related genes were determined by quantitative real-time polymerase chain reaction [qRT-PCR]. The phosphatidylinositol 3-kinase [PI3K]/protein kinase B [Akt] signaling pathwayassociated protein expressions were examined using Western blot. After osteoblasts were transfected with protein tyrosine phosphatase non-receptor type 2 [PTPN2] overexpression plasmid, the impact of PTPN2 on osteoblasts treated with AS-IV was examined.</p><p><strong>Results: </strong>AS-IV treatment enhanced osteogenic differentiation and up-regulated the expression of osteogenic differentiation-related genes, as well as the levels of p- PI3K/PI3K and p-AKT/AKT, while reducing PTEN protein production in osteoblasts. Overexpression of phosphatase and tensin homolog [PTEN] inhibited osteogenic differentiation, and PTPN2 overexpression counteracted the effects of AS-IV on osteogenic differentiation.</p><p><strong>Conclusion: </strong>AS-IV contributing to osteogenic differentiation may be related to the PTPN2-mediated PTEN/PI3K/Akt pathway.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.2000,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current molecular medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/0115665240333454241203050356","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
Abstract
Background: This study focuses on exploring the impact of Astragaloside IV [AS-IV] on osteogenic differentiation.
Methods: Osteogenic differentiation was induced in rat osteoblasts, following which treatment with AS-IV at varied doses was performed. Using Alizarin red staining and alkaline phosphatase [ALP] detection assay, the osteogenic differentiation of the cells was investigated. The expressions of osteogenic differentiation-related genes were determined by quantitative real-time polymerase chain reaction [qRT-PCR]. The phosphatidylinositol 3-kinase [PI3K]/protein kinase B [Akt] signaling pathwayassociated protein expressions were examined using Western blot. After osteoblasts were transfected with protein tyrosine phosphatase non-receptor type 2 [PTPN2] overexpression plasmid, the impact of PTPN2 on osteoblasts treated with AS-IV was examined.
Results: AS-IV treatment enhanced osteogenic differentiation and up-regulated the expression of osteogenic differentiation-related genes, as well as the levels of p- PI3K/PI3K and p-AKT/AKT, while reducing PTEN protein production in osteoblasts. Overexpression of phosphatase and tensin homolog [PTEN] inhibited osteogenic differentiation, and PTPN2 overexpression counteracted the effects of AS-IV on osteogenic differentiation.
Conclusion: AS-IV contributing to osteogenic differentiation may be related to the PTPN2-mediated PTEN/PI3K/Akt pathway.
期刊介绍：
Current Molecular Medicine is an interdisciplinary journal focused on providing the readership with current and comprehensive reviews/ mini-reviews, original research articles, short communications/letters and drug clinical trial studies on fundamental molecular mechanisms of disease pathogenesis, the development of molecular-diagnosis and/or novel approaches to rational treatment. The reviews should be of significant interest to basic researchers and clinical investigators in molecular medicine. Periodically the journal invites guest editors to devote an issue on a basic research area that shows promise to advance our understanding of the molecular mechanism(s) of a disease or has potential for clinical applications.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
