中国临床药理学与治疗学2013，Vol.18Issue(2)：161-165,5.
冬凌草甲素通过PI3K/Akt通路诱导MDA-MB-231细胞的凋亡
Oridonin induces MDA-MB-231 cells apoptosis through PI3K/Akt pathway in vitro
摘要
Abstract
AIM: To research the proliferation inhibitory effect of oridonin on human breast cancer MDA-MB-231 cells and explore the mech anism of the inhibitory effect.METHODS: MDA-MB-231 cells were incubated with oridonin in vitro.Morphological changes of MDA-MB-231 cells induced by oridonin for 24 h were ob served by invert microscrope.The cell viability rate was evaluated by MTT assay.The cell ap-optotic rate was evalutated by flow cytometry (FCM).The apoptosis associated protein level of procaspase-3, PARP,Akt, p-Akt, p-GSK 3β was examined by Western blotting.RESULTS: The apoptosis phenomenon of MDA-MB-231 cells induced by oridonin for 24 h could be ob served.The apoptosis phenomenon of 24 μmol/ L group was more obvious than other groups.The cell viability rate induced by 6,12,24 μmol/ L oridonin was decreased and apoptotic rate was increased in a time- and dose-dependent manner (P<0.01).Oridonin cleaved PARP which is the substrate of caspase-3 in a dose-dependent manner(P<0.05).Oridonin also down- regula ted the protein level of procaspase-3, phospho-Akt(p-Akt) and phospho-GSK3β (p- GSK3β) in a dose-dependent manner(P<0.05).CONCLU SION: Oridonin can inhibit the proliferation of human breast cancer MDA-MB-231 cells and in duce cell apoptosis by inhibiting PI3K/Akt path way.关键词
冬凌草甲素/MDA-MB-231细胞/细胞凋亡Key words
Oridonin/MDA-MB-231/Cell apoptosis分类
医药卫生引用本文复制引用
汪茗,章尧,谢向荣,戚之琳,毕富勇..冬凌草甲素通过PI3K/Akt通路诱导MDA-MB-231细胞的凋亡[J].中国临床药理学与治疗学,2013,18(2):161-165,5.基金项目
安徽省高校省级优秀青年人才基金项目(2011SQRL104) （2011SQRL104）
安徽省高校省级自然科学研究项目(KJ20112383) （KJ20112383）
皖南医学院中青年科研基金资助项目(WK201010) （WK201010）
