标题:Diosgenin induces apoptosis in IGF-1-stimulated human thyrocytes through two caspase-dependent pathways
作者:Mu,S.;Tian,X.;Ruan,Y.;Liu,Y.;Bian,D.;Ma,C.;Yu,C.;Feng,M.;Wang,F.;Gao,L.;Zhao,J.-J.
作者机构:[Mu, S] Provincial Hospital Affiliated to Shandong University, Jinan 250021, China, Hospital Affiliated to Shandong Traditional Chinese Medicine Unive 更多
通讯作者:Zhao, JJ
通讯作者地址:[Zhao, JJ]324 Jing 5 Rd, Jinan 250021, Peoples R China.
来源:Biochemical and Biophysical Research Communications
出版年:2012
卷:418
期:2
页码:347-352
DOI:10.1016/j.bbrc.2012.01.024
关键词:Apoptosis;Caspase-dependent pathways;Diosgenin;IGF-1;Primary human thyrocytes
摘要:Insulin-like growth factor-1 (IGF-1) is a growth factor of the thyroid that has been shown in our previous study to possess proliferative and antiapoptotic effects in FRTL-5 cell lines through the upregulation of cyclin D and Fas-associated death domain-like interleukin-1-converting enzyme (FLICE)-inhibitory protein (FLIP). Diosgenin, a natural steroid sapogenin from plants, has been shown to induce apoptosis in many cell lines, with the exception of thyroid cells. In this report, we investigated the apoptotic effect and mechanism of diosgenin in IGF-1-stimulated primary human thyrocytes. Primary human thyrocytes were preincubated with or without IGF-1 for 24. h and subsequently exposed to varying concentrations of diosgenin for different times. We found that diosgenin induced apoptosis in human thyrocytes pretreated with IGF-1 in a dose-dependent manner through the activation of caspase cascades. Moreover, diosgenin inhibited FLIP and activated caspase-8 in the FAS-related apoptotic pathway. Diosgenin increased the production of ROS, regulated the balance of Bax and Bcl-2 and cleaved caspase-9 in the mitochondrial apoptotic pathway. These results indicate that diosgenin induces apoptosis in IGF-1-stimulated primary human thyrocytes through two caspase-dependent pathways.
收录类别:SCOPUS;SCIE
WOS核心被引频次:7
Scopus被引频次:8
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84862781022&doi=10.1016%2fj.bbrc.2012.01.024&partnerID=40&md5=43f807b5ba2e76de6b3e019ac02d87e0
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