摘要
目的探讨抗P gp单抗UIC2对X射线照射后不同时间肿瘤细胞凋亡、细胞内cytochromec(Cyt c)释放和caspase3活性的影响。方法以抗P gp单抗UIC2抑制P gp功能,X射线照射P gp表达的乳腺癌耐药细胞MCF7Adr。运用流式细胞仪检测X射线照射后细胞凋亡、细胞内Cyt c和caspase3活性的变化。结果X射线照射后6、12和24h应用UIC2抑制P gp功能组细胞凋亡显著增加(P<0.01),胞浆Cyt c的表达均明显高于对照组(P<0.05),胞内caspase3活性均显著高于对照组(P<0.01)。结论抑制P gp功能,增加了Cyt c释放和caspase3活性,提示P gp对X射线照射后肿瘤细胞胞浆Cyt c释放和caspase3活性均有抑制作用。
Objective To investigate the effects of P-glycoprotein （P-gp） on cytochrome c （Cyt c） release and caspase-3 activation in drug-resistant tumor cell after X-ray irradiation. Methods Anti-P-gp McAb UIC-2 was applied to block P-gp function. MCF-7/Adr, P-gp-overexpressed drug-resistant breast cancer cell line, was irradiated by X-rays. Flow cytometry was used to measure apoptosis, dynamic changes of mitochondrial cytoehrome c release and caspase-3 activation at various time after X-ray irradiation. Results Both the expression of cyt c and the activation of caspase-3 in P-gp-bloeked group were up-regulated significantly, compared with those in control group at 6 h, 12 h, and 24 h after X-ray irradiation, respectively. Conclusion The current study showed that inhibition of P-gp function can increase cytochrome c release and caspase-3 activation. It suggested that P-gp inhibits X-ray induced cytochrome c release and caspase-3 activation.
出处
《中华放射医学与防护杂志》
CAS
CSCD
北大核心
2006年第2期118-120,共3页
Chinese Journal of Radiological Medicine and Protection
基金
国家自然科学基金资助项目(30100045)
