摘要
目的:探讨IκB-α磷酸化抑制剂Bay117082特异性阻断NFκB信号转导途径对羟基喜树碱(HCPT)诱导Bcap37细胞凋亡的影响。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调亡;Western blot研究细胞调亡所涉及的蛋白表达;DIG-EMSA研究NFκB/DNA结合状况。结果:5μmol.L-1Bay117082可以抑制HCPT对IκB-α的磷酸化,阻断NFκB信号转导途径,阻滞HCPT诱导的细胞凋亡,同时也抑制HCPT诱导pro-Caspase3和Bcl-2的降解。结论:Bay117082对HCPT诱导的乳腺癌细胞凋亡有明显的抑制作用,其作用机制与NFκB信号转导途径有关,NFκB起促进凋亡的作用。
AIM: To investigate the role of Bay117082 in apoptosis induced by 10-Hydroxycamptothecin (HCPT) in human breast carcinoma cells. METHODS: The cell growth inhibiting was measured by MTT assay, agarose gel eletrophoresis were performed for cell apoptosis, Western Blotting were performed for protein expression. DIG-EMSA was conducted to determine the DNA-binding activation of NF kB. RESULTS: 5mmol· L^-1 Bay117082 had a remarkable inhibition on apoptosis induced by HCPF in breast cancer cells. NF kB was not activated after exposing to HCPT plus Bay117082. Pro-Caspase3 and Bcl-2 were not degraded either. CONCLUSION: Bay117082 may attenuate apoptosis induced by HCPT through inhibiting activation of NF kB in Bcap37 cell line.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2005年第7期755-759,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics