Protective effect and mechanisms of ginsenoside Rg1 against MDA-suppressed proliferation in mesenchymal stem cells derived from murine bone marrow

Ye Li, Cheng Ma, Z. Lv, Changhai Shao, Jun Zhang, Wenye Geng, Lan Zheng
{"title":"Protective effect and mechanisms of ginsenoside Rg1 against MDA-suppressed proliferation in mesenchymal stem cells derived from murine bone marrow","authors":"Ye Li, Cheng Ma, Z. Lv, Changhai Shao, Jun Zhang, Wenye Geng, Lan Zheng","doi":"10.1142/S2575900019500083","DOIUrl":null,"url":null,"abstract":"Objective: The present study was designed to investigate the cytoprotective effects of ginsenoside Rg1 (GS-Rg1) against malondialdehyde (MDA)-suppressed proliferation of the mesenchymal stem cells (MSCs) and its possible mechanisms in vitro. Methods: Murine bone marrow-derived MSCs were treated with GS-Rg1 (10, 50, 100[Formula: see text]mg/L) for 24[Formula: see text]h before being incubated with MDA in vitro, CFU-Fassay, the cell viability and BrdU incorporation assay were examined, the expression of cyclin-dependent kinase 2 (CDK2), p21 and cyclin E of MSC were examined by Q-RT-PCR and Western blotting. Results: The results showed that the number and size of murine bone marrow MSC colonies, the number of colony-forming cells, methyl thiazolyltetrazolium (MTT) absorbed value greatly and percentage of BrdU-positive cells increased significantly in MSC pretreated with GS-Rg1. GS-Rgl pretreatment markedly decreased the expression level of p21 and increased the expression of CDK2 and cyclin E. GS-Rg1 protects MSCs from MDA-suppressed proliferation. Conclusion: The protective mechanism could be related to its ability to increase the expression of CDK2 and cyclin E, and to reduce the expression of p21.","PeriodicalId":23184,"journal":{"name":"Traditional Medicine and Modern Medicine","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1142/S2575900019500083","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Traditional Medicine and Modern Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1142/S2575900019500083","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Objective: The present study was designed to investigate the cytoprotective effects of ginsenoside Rg1 (GS-Rg1) against malondialdehyde (MDA)-suppressed proliferation of the mesenchymal stem cells (MSCs) and its possible mechanisms in vitro. Methods: Murine bone marrow-derived MSCs were treated with GS-Rg1 (10, 50, 100[Formula: see text]mg/L) for 24[Formula: see text]h before being incubated with MDA in vitro, CFU-Fassay, the cell viability and BrdU incorporation assay were examined, the expression of cyclin-dependent kinase 2 (CDK2), p21 and cyclin E of MSC were examined by Q-RT-PCR and Western blotting. Results: The results showed that the number and size of murine bone marrow MSC colonies, the number of colony-forming cells, methyl thiazolyltetrazolium (MTT) absorbed value greatly and percentage of BrdU-positive cells increased significantly in MSC pretreated with GS-Rg1. GS-Rgl pretreatment markedly decreased the expression level of p21 and increased the expression of CDK2 and cyclin E. GS-Rg1 protects MSCs from MDA-suppressed proliferation. Conclusion: The protective mechanism could be related to its ability to increase the expression of CDK2 and cyclin E, and to reduce the expression of p21.
人参皂苷Rg1对小鼠骨髓间充质干细胞MDA抑制增殖的保护作用及其机制
目的:研究人参皂苷Rg1 (GS-Rg1)对丙二醛(MDA)抑制间充质干细胞(MSCs)增殖的体外保护作用及其可能机制。方法:用GS-Rg1(10、50、100[公式:见文]mg/L)处理小鼠骨髓源性间充质干细胞24 h后,与MDA体外孵育,检测CFU-Fassay、细胞活力和BrdU结合实验,采用Q-RT-PCR和Western blotting检测MSC细胞周期蛋白依赖性激酶2 (CDK2)、p21和细胞周期蛋白E的表达。结果:GS-Rg1预处理小鼠骨髓间充质干细胞后,小鼠骨髓间充质干细胞的集落数量、大小、集落形成细胞数量、甲基噻唑四氮唑(MTT)吸收值和brdu阳性细胞比例均显著增加。GS-Rg1预处理可显著降低p21的表达水平,增加CDK2和cyclin e的表达,使MSCs免受mda抑制的增殖。结论:其保护机制可能与其提高CDK2和cyclin E的表达,降低p21的表达有关。
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 求助全文
来源期刊
自引率
0.00%
发文量
5
审稿时长
12 weeks
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信