中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2013年
8期
1649-1651
,共3页
何庆良%周俊峰%潘敦%黄发昆%石铮%王家兴
何慶良%週俊峰%潘敦%黃髮昆%石錚%王傢興
하경량%주준봉%반돈%황발곤%석쟁%왕가흥
胆管癌%大黄素%磷酸肌醇3激酶/蛋白激酶B/雷帕霉素靶蛋白信号通路
膽管癌%大黃素%燐痠肌醇3激酶/蛋白激酶B/雷帕黴素靶蛋白信號通路
담관암%대황소%린산기순3격매/단백격매B/뢰파매소파단백신호통로
Cholangiocarcinoma%Emodin%Phosphatidylinositol 3 kinase/protein kinase B/mammalian target of rapamycin
目的 观察大黄素在体外对胆管癌QBC939细胞生长的抑制作用及其对磷酸肌醇3激酶(PI3K)/蛋白激酶B(Akt)/雷帕霉素靶蛋白(mTOR)信号转导通路的影响.方法 用大黄素作为干预因素,时间效应组以含大黄素的培养液分别培养QBC939细胞不同时间,剂量效应组分别用不同浓度大黄素的培养液与QBC939细胞共培养;检测细胞增殖,逆转录-聚合酶链反应(RT-PCR)检测细胞中B淋巴细胞/白血病-2 (bcl-2) mRNA表达,Western blot检测细胞中bcl-2、Akt、磷酸化Akt (p-Akt)、核因子(NF)-κB、磷酸化NF-κB(p-NF-κB)、mTOR、磷酸化mTOR(p-mTOR)蛋白质的表达.结果 10、20、40、80 μmol/L大黄素对QBC939细胞增殖抑制率分别为17.3%、28.6%、46.5%和66.4% (P <0.05),bcl-2、p-Akt、NF-κB、p-NF-κB、mTOR、p-mTOR表达明显下降,Akt表达无变化.结论 大黄素抑制QBC939细胞增殖,可能通过抑制PI3K/Akt/mTOR信号转导途径.
目的 觀察大黃素在體外對膽管癌QBC939細胞生長的抑製作用及其對燐痠肌醇3激酶(PI3K)/蛋白激酶B(Akt)/雷帕黴素靶蛋白(mTOR)信號轉導通路的影響.方法 用大黃素作為榦預因素,時間效應組以含大黃素的培養液分彆培養QBC939細胞不同時間,劑量效應組分彆用不同濃度大黃素的培養液與QBC939細胞共培養;檢測細胞增殖,逆轉錄-聚閤酶鏈反應(RT-PCR)檢測細胞中B淋巴細胞/白血病-2 (bcl-2) mRNA錶達,Western blot檢測細胞中bcl-2、Akt、燐痠化Akt (p-Akt)、覈因子(NF)-κB、燐痠化NF-κB(p-NF-κB)、mTOR、燐痠化mTOR(p-mTOR)蛋白質的錶達.結果 10、20、40、80 μmol/L大黃素對QBC939細胞增殖抑製率分彆為17.3%、28.6%、46.5%和66.4% (P <0.05),bcl-2、p-Akt、NF-κB、p-NF-κB、mTOR、p-mTOR錶達明顯下降,Akt錶達無變化.結論 大黃素抑製QBC939細胞增殖,可能通過抑製PI3K/Akt/mTOR信號轉導途徑.
목적 관찰대황소재체외대담관암QBC939세포생장적억제작용급기대린산기순3격매(PI3K)/단백격매B(Akt)/뢰파매소파단백(mTOR)신호전도통로적영향.방법 용대황소작위간예인소,시간효응조이함대황소적배양액분별배양QBC939세포불동시간,제량효응조분별용불동농도대황소적배양액여QBC939세포공배양;검측세포증식,역전록-취합매련반응(RT-PCR)검측세포중B림파세포/백혈병-2 (bcl-2) mRNA표체,Western blot검측세포중bcl-2、Akt、린산화Akt (p-Akt)、핵인자(NF)-κB、린산화NF-κB(p-NF-κB)、mTOR、린산화mTOR(p-mTOR)단백질적표체.결과 10、20、40、80 μmol/L대황소대QBC939세포증식억제솔분별위17.3%、28.6%、46.5%화66.4% (P <0.05),bcl-2、p-Akt、NF-κB、p-NF-κB、mTOR、p-mTOR표체명현하강,Akt표체무변화.결론 대황소억제QBC939세포증식,가능통과억제PI3K/Akt/mTOR신호전도도경.
Objective To investigate the effects of Emodin on proliferation inhibition of cholangiocarcinoma QBC939 cells and phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) in vitro.Methods QBC939 cells were cultured with Emodin for different time periods,or with different concentrations of Emodin.The proliferation inhibition of cholangiocarcinoma QBC939 cells was detected by using methyl thiazol tetrazolium (MTT) assay.The expression of B lymphocytes/leukemia-2 (bcl-2) mRNA and protein was detected by using reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting.Akt,p-Akt,nuclear factor-κB (NF-κB),phosphorylated NF-κB (p-NF-κB),mTOR,and phosphorylated mTOR (p-mTOR) were examined by using Western blotting.Results Inhibitory rate of QBC939 cells treated with 10,20,40 and 80 μmol/L Emodin for 48 h was 17.3%,28.6%,46.5%,and 66.4% respectively (P <0.05).Emodin could down-regulate the expression levels of bcl-2,p-Akt,NF-κB,p-NF-κB,mTOR and p-mTOR (P < 0.05),but had no signficnat effect on the Akt expression.Conclusion Emodin can inhibit proliferation of QBC939 cells probably by down-regulating PI3K/Akt/mTOR.