Caspase 3抑制剂抑制羟基喜树碱对人乳腺癌Bcap37细胞NF-κB的激活  

Caspase 3 inhibitor Ac-DEVD-CHO attenuates 10-hydroxycamptoth-ecin-induced activation of NF-κB in Bcap37 cells

作　　者：叶孟[1] 林蕾[2] 潘宏铭[3] 方勇[3] 吴金民[3] 

机构地区：[1]宁波大学附属医院肿瘤科,浙江宁波315020 [2]宁波大学附属医院皮肤科,浙江宁波315020 [3]浙江大学附属邵逸夫医院肿瘤中心,浙江杭州310016

出　　处：《中国病理生理杂志》2007年第8期1508-1511,共4页Chinese Journal of Pathophysiology

基　　金：宁波市医学科研计划资助(No.200529);宁波市博士基金资助(No.2005A610020)

摘　　要：目的:探讨caspase 3抑制剂Ac-DEVD-CHO对caspase 3和NF-κB信号转导途径的影响。方法:采用MTT法测定细胞的增殖活力,琼脂糖凝胶电泳观察细胞凋亡,流式细胞仪进行细胞周期分析,Westernblotting和DIG-EMSA研究细胞凋亡途径。结果:Caspase 3抑制剂Ac-DEVD-CHO可抑制羟基喜树碱(HCPT)对Bcap-37诱导的凋亡,抑制Pro-caspase 3的裂解,并能抑制IκBα蛋白降解,阻止NF-κB活化。结论:Caspase 3抑制剂Ac-DEVD-CHO除特异性抑制Pro-caspase 3的裂解外,还可以抑制HCPT对Bcap37细胞NF-κB的活化。AIM ： To investigate the role of caspase 3 inhibitor Ac - DEVD - CHO in caspase 3 signaling pathway and NF -κB activation induced by 10 - hydroxycamptothecin （HCPT） in human breast carcinoma cells. METHODS： The cell growth inhibition was measured by MTT assay. Agarose gel electrophoresis was performed for detecting cell apeptosis. Western blotting was used for determining protein expression. DIG - EMSA was conducted to measure the DNA - binding activation of NF -κB. RESULTS ： Caspase 3 inhibitor Ae - DEVD - CHO attenuated HCPT - induced apoptosis in human breast carcinoma. Ae - DEVD - CHO also suppressed the degradation of easpase 3 and IκBα, and arrested the activation of NF -κB. CONCLUSION： Caspase 3 inhibitor Ae - DEVD - CHO regulates the activation of easpase 3 and NF -κB, and attenuates apoptosis in Bcap37 cell line induced by HCPT.

关 键 词：喜树碱 半胱氨酸天冬氨酸蛋白酶3抑制剂 细胞凋亡 NF—κB 

分 类 号：R363[医药卫生—病理学]