解剖学报
解剖學報
해부학보
ACTA ANATOMICA SINICA
2001年
2期
155-158
,共4页
戴书静%王继峰%莫日根%郭顺根%牛建昭
戴書靜%王繼峰%莫日根%郭順根%牛建昭
대서정%왕계봉%막일근%곽순근%우건소
去甲斑蝥素(NCTD)%NF-κB%IκBα核转录因子
去甲斑蝥素(NCTD)%NF-κB%IκBα覈轉錄因子
거갑반모소(NCTD)%NF-κB%IκBα핵전록인자
从核转录因子NF-κB和其抑制分子IκBα的相互作用揭示去甲斑蝥素的抗肿瘤作用机理，为其进一步开发利用提供理论依据。 方法 选用人肝癌细胞株(Bel7402)，常规培养，分为细胞对照组及去甲斑蝥素不同浓度组，进行细胞生长曲线测定、细胞集落形成实验及MTT实验；同时对细胞进行Giemsa染色、免疫细胞化学染色(一抗分别为anti-p65、anti-IκBα)。Westernblot检测IκBα的表达。 结果 生长曲线测定，细胞集落形成实验及MTT实验结果表明，去甲斑蝥素对人肝癌细胞株的生长有明显的抑制作用；免疫细胞化学及Westernblot结果显示：去甲斑蝥素可增强细胞内IκBα的表达，并抑制NF-κB的表达与活性。 结论 去甲斑蝥素有良好的抗肿瘤效应，其作用机理可能与其能增强核转录因子NF-κB的抑制分子IκBα的表达有关。
從覈轉錄因子NF-κB和其抑製分子IκBα的相互作用揭示去甲斑蝥素的抗腫瘤作用機理，為其進一步開髮利用提供理論依據。 方法 選用人肝癌細胞株(Bel7402)，常規培養，分為細胞對照組及去甲斑蝥素不同濃度組，進行細胞生長麯線測定、細胞集落形成實驗及MTT實驗；同時對細胞進行Giemsa染色、免疫細胞化學染色(一抗分彆為anti-p65、anti-IκBα)。Westernblot檢測IκBα的錶達。 結果 生長麯線測定，細胞集落形成實驗及MTT實驗結果錶明，去甲斑蝥素對人肝癌細胞株的生長有明顯的抑製作用；免疫細胞化學及Westernblot結果顯示：去甲斑蝥素可增彊細胞內IκBα的錶達，併抑製NF-κB的錶達與活性。 結論 去甲斑蝥素有良好的抗腫瘤效應，其作用機理可能與其能增彊覈轉錄因子NF-κB的抑製分子IκBα的錶達有關。
종핵전록인자NF-κB화기억제분자IκBα적상호작용게시거갑반모소적항종류작용궤리，위기진일보개발이용제공이론의거。 방법 선용인간암세포주(Bel7402)，상규배양，분위세포대조조급거갑반모소불동농도조，진행세포생장곡선측정、세포집락형성실험급MTT실험；동시대세포진행Giemsa염색、면역세포화학염색(일항분별위anti-p65、anti-IκBα)。Westernblot검측IκBα적표체。 결과 생장곡선측정，세포집락형성실험급MTT실험결과표명，거갑반모소대인간암세포주적생장유명현적억제작용；면역세포화학급Westernblot결과현시：거갑반모소가증강세포내IκBα적표체，병억제NF-κB적표체여활성。 결론 거갑반모소유량호적항종류효응，기작용궤리가능여기능증강핵전록인자NF-κB적억제분자IκBα적표체유관。
Objective In order to study the antitumor mechanism of norcantharidin(NCTD),the effects of NCTD on nuclear transcription factor kappa B(NF-κB) and the inhibitor of NF-κB(IκBα) of the human hepatic carcinoma cells (Bel 7402) were investigated. Methods Exponentially growing Bel 7402 cells were used for plotting the growth curve,detecting the ability of forming cell colony and MTT test.Cel ls were stained by Giemsa,and used for detecting the expression of p65(a subunit of NF-κB) and IκBα by immunocytochemical method and Western blot.Results Addition into the culture,NCTD inhibited the growth of Bel 7402 i n a concentration-and incubation time-dependent manner.Immunocytochemical stai n and Western blot showed that NCTD enhanced the expression of IκBα in cells o bviously. Conclusion NCTD inhibited the proliferation of Bel 7402 cells in a dose-and time-dependent manner.The mechanism may be related to the increasin g expression of IκBα,the inhibitor of NF-κB,sequentially suppress the activi ty of NF-κB,which is necessary for the survival of tumor cells.
