中华器官移植杂志
中華器官移植雜誌
중화기관이식잡지
CHINESE JOURNAL OF ORGAN TRANSPLANTATION
2009年
1期
26-29
,共4页
涂金鹏%郑虹%张晓东%叶丽虹%沈中阳
塗金鵬%鄭虹%張曉東%葉麗虹%瀋中暘
도금붕%정홍%장효동%협려홍%침중양
癌%肝细胞%糖皮质激素类%细胞增殖
癌%肝細胞%糖皮質激素類%細胞增殖
암%간세포%당피질격소류%세포증식
Carcinoma,hepatocellular%Glucocortieoids%Cell proliferation
目的 探讨糖皮质激素在体外环境下对肝癌细胞增殖的影响及可能机制.方法 以不同浓度(0.1、0.01、1×10-3、1×10-4、1×10-5、1×10～mmol/L,均为终浓度)的地塞米松(Dex)在体外作用于人肝癌细胞系Bel7402、H7402和Hep G2细胞,计算细胞生长抑制率.再以Bel7402细胞为对象,分别加入1×10-4 mmol/L的Dex(Dex组)、1×10-4mmol/L的Ru486(Ru486组)、Dex和Ru486(浓度均为1×10-4mmol/L,Dex+Ru486组),并设加人培养液的阴性对照组,计算各组细胞生长抑制率,流式细胞仪测定各组的细胞周期分布,Western免疫印迹法检测Bel7402细胞的P21蛋白的表达;报告基因法检测Dex和Ru486对Bel7402细胞的核因子κB(NF-κB)启动子的影响.结果 各浓度Dex对3种肝癌细胞的增殖均有抑制作用,且呈浓度依赖性.Dex组Bel7402细胞的增殖受到抑制,其G0/G1期细胞增多,S期细胞减少,其细胞内的P21蛋白表达上调,NF-κB启动子的激活受到抑制,而加入Ru486后(Dex+Ru486组),Dex的这些作用被逆转.结论 Dex可以抑制Bel7402细胞的增殖,并使细胞周期停滞在G上/G1,期,其机制可能包括上调P21蛋白的表达和抑制NF-κB的表达,这种作用由糖皮质激素胞内受体介导.
目的 探討糖皮質激素在體外環境下對肝癌細胞增殖的影響及可能機製.方法 以不同濃度(0.1、0.01、1×10-3、1×10-4、1×10-5、1×10～mmol/L,均為終濃度)的地塞米鬆(Dex)在體外作用于人肝癌細胞繫Bel7402、H7402和Hep G2細胞,計算細胞生長抑製率.再以Bel7402細胞為對象,分彆加入1×10-4 mmol/L的Dex(Dex組)、1×10-4mmol/L的Ru486(Ru486組)、Dex和Ru486(濃度均為1×10-4mmol/L,Dex+Ru486組),併設加人培養液的陰性對照組,計算各組細胞生長抑製率,流式細胞儀測定各組的細胞週期分佈,Western免疫印跡法檢測Bel7402細胞的P21蛋白的錶達;報告基因法檢測Dex和Ru486對Bel7402細胞的覈因子κB(NF-κB)啟動子的影響.結果 各濃度Dex對3種肝癌細胞的增殖均有抑製作用,且呈濃度依賴性.Dex組Bel7402細胞的增殖受到抑製,其G0/G1期細胞增多,S期細胞減少,其細胞內的P21蛋白錶達上調,NF-κB啟動子的激活受到抑製,而加入Ru486後(Dex+Ru486組),Dex的這些作用被逆轉.結論 Dex可以抑製Bel7402細胞的增殖,併使細胞週期停滯在G上/G1,期,其機製可能包括上調P21蛋白的錶達和抑製NF-κB的錶達,這種作用由糖皮質激素胞內受體介導.
목적 탐토당피질격소재체외배경하대간암세포증식적영향급가능궤제.방법 이불동농도(0.1、0.01、1×10-3、1×10-4、1×10-5、1×10～mmol/L,균위종농도)적지새미송(Dex)재체외작용우인간암세포계Bel7402、H7402화Hep G2세포,계산세포생장억제솔.재이Bel7402세포위대상,분별가입1×10-4 mmol/L적Dex(Dex조)、1×10-4mmol/L적Ru486(Ru486조)、Dex화Ru486(농도균위1×10-4mmol/L,Dex+Ru486조),병설가인배양액적음성대조조,계산각조세포생장억제솔,류식세포의측정각조적세포주기분포,Western면역인적법검측Bel7402세포적P21단백적표체;보고기인법검측Dex화Ru486대Bel7402세포적핵인자κB(NF-κB)계동자적영향.결과 각농도Dex대3충간암세포적증식균유억제작용,차정농도의뢰성.Dex조Bel7402세포적증식수도억제,기G0/G1기세포증다,S기세포감소,기세포내적P21단백표체상조,NF-κB계동자적격활수도억제,이가입Ru486후(Dex+Ru486조),Dex적저사작용피역전.결론 Dex가이억제Bel7402세포적증식,병사세포주기정체재G상/G1,기,기궤제가능포괄상조P21단백적표체화억제NF-κB적표체,저충작용유당피질격소포내수체개도.
Objective To illustrate the role of glucocorticoids in growth regulation of human hepatoma cells and the possible mechanism. Methods The human hepatoma carcinoma cell lines Be17402, H7402 and Hep G2 were treated with different concentrations of dexamethasones (Dex) (0.1, 0.01, 1×10-3, 1×10-4, 1×10-5, and 1×10-6 mmol/L). The inhibition rate was calculated. Be17402 cells were treated with Dex (1×10-4 mmol/L, Dex group), or RU486 (1×10-4 mmol/L, RU486 group) or both (both concentrations were 1×10-4 mmol/L, Dex+ Ru486 group), or medium as negative control group. The inhibition rate was calculated, and the cycle progression was measured by flow cytometry. Western blot was used to detect the expression of P21 protein, and the reporter genes were employed to detect the effect of Dex and Ru486 on promoter of NF-kappa B in Be17402 cells. Results Dex could significantly inhibit the proliferation of these cells in a dose-dependent manner. Dex inhibited the growth of Be17402, and induced G0/G1 arrest. Dex increased the expression of P21, and suppressed the promoter of NF-kappa B. Ru486 could reverse these effects. Conclusion Up-regulation of P21/WAF1 expression and suppression of promoter of NF-κB may contribute to the growth inhibition and G0/G1 arrest induced by glucocorticoid in human hepatoma carcinoma cells. These effects may be mediated by GR.
