中国医学创新
中國醫學創新
중국의학창신
MEDICAL INNOVATION OF CHINA
2015年
4期
14-17
,共4页
胰腺肿瘤%凋亡%NF-κB
胰腺腫瘤%凋亡%NF-κB
이선종류%조망%NF-κB
Pancreatic neoplasm%Apoptosis%NF-κB
目的：观察特异性阻断NF-κB信号通路对人胰腺癌SW1990细胞增殖和凋亡的影响并探讨其可能的分子机制。方法：SW1990细胞经不同浓度（2.5μmol/L、5μmol/L和10μmol/L）特异性NF-κB通路阻断剂Bay 11-7082处理后，光学显微镜和荧光显微镜下观察SW1990细胞形态学变化；cck-8法测Bay 11-7082对胰腺癌细胞生长情况的影响；流式细胞术观察细胞凋亡；western印迹检测细胞中caspase-3和Bax表达的变化。结果：Bay 11-7082可抑制胰腺癌SW1990细胞生长，其作用呈剂量依赖性；Bay 11-7082处理后凋亡胰腺癌细胞呈剂量依赖性增加；随着Bay 11-7082剂量的增加，细胞中caspase-3和Bax表达水平上调。结论：Bay 11-7082对胰腺癌细胞有一定增殖抑制和诱导细胞凋亡的作用，诱导细胞凋亡可能是其增殖抑制的主要作用方式，其机制可能为通过活化caspase-3和上调Bax的表达实现。
目的：觀察特異性阻斷NF-κB信號通路對人胰腺癌SW1990細胞增殖和凋亡的影響併探討其可能的分子機製。方法：SW1990細胞經不同濃度（2.5μmol/L、5μmol/L和10μmol/L）特異性NF-κB通路阻斷劑Bay 11-7082處理後，光學顯微鏡和熒光顯微鏡下觀察SW1990細胞形態學變化；cck-8法測Bay 11-7082對胰腺癌細胞生長情況的影響；流式細胞術觀察細胞凋亡；western印跡檢測細胞中caspase-3和Bax錶達的變化。結果：Bay 11-7082可抑製胰腺癌SW1990細胞生長，其作用呈劑量依賴性；Bay 11-7082處理後凋亡胰腺癌細胞呈劑量依賴性增加；隨著Bay 11-7082劑量的增加，細胞中caspase-3和Bax錶達水平上調。結論：Bay 11-7082對胰腺癌細胞有一定增殖抑製和誘導細胞凋亡的作用，誘導細胞凋亡可能是其增殖抑製的主要作用方式，其機製可能為通過活化caspase-3和上調Bax的錶達實現。
목적：관찰특이성조단NF-κB신호통로대인이선암SW1990세포증식화조망적영향병탐토기가능적분자궤제。방법：SW1990세포경불동농도（2.5μmol/L、5μmol/L화10μmol/L）특이성NF-κB통로조단제Bay 11-7082처리후，광학현미경화형광현미경하관찰SW1990세포형태학변화；cck-8법측Bay 11-7082대이선암세포생장정황적영향；류식세포술관찰세포조망；western인적검측세포중caspase-3화Bax표체적변화。결과：Bay 11-7082가억제이선암SW1990세포생장，기작용정제량의뢰성；Bay 11-7082처리후조망이선암세포정제량의뢰성증가；수착Bay 11-7082제량적증가，세포중caspase-3화Bax표체수평상조。결론：Bay 11-7082대이선암세포유일정증식억제화유도세포조망적작용，유도세포조망가능시기증식억제적주요작용방식，기궤제가능위통과활화caspase-3화상조Bax적표체실현。
Objective:To study the effect of blocking the NF-κB signaling pathway on proliferation and apoptosis in human pancreatic cancer cell line SW1990 and its possible mechanism.Method:SW1990 cells were treated with different concentrations of NF-κB inhibitor Bay 11-7082(2.5μmol/L,5μmol/L 和 10μmol/L),SW1990 cells morphological changes after treatment were observed under the optical microscope and fluorescence microscopy.CCK-8 assay was used to evaluate the growth influence of Bay 11-7082 on pancreatic cancer SW1990 cells,the flow cytometry was used to determine apoptosis in SW1990 cells.Western blot was used to detect the protein expression of caspase-3 and Bax.Result:A dose-dependent inhibitory effect of Bay 11-7082 on pancreatic cancer SW1990 cells was observed.The result of FCM indicated that treated with Bay 11-7082 exhibited a significant increase of apoptosis in a dose-dependent manner.The expression of caspase-3 and Bax was up-regulated in human pancreatic cancer SW1990 cells after treatment. Conclusion:Bay 11-7082 inhibits the proliferation of SW1990 cells,which is mediated by altering apoptosis-related genes through up-regulation of caspase-3 and Bax.
