腺苷A3受体激活对柔红霉素血管内皮细胞毒性的保护作用及其机制研究  

Activation of adenosine A3 receptor protecting vascular endothelial cells from daunomycin toxicity

作　　者：杨赛男[1] 陈润[1] 陈洁平[1] 裴莉[1] 

机构地区：[1]第三军医大学西南医院血液科,重庆400038

出　　处：《临床血液学杂志》2015年第3期396-398,共3页Journal of Clinical Hematology

摘　　要：目的:观察腺苷A3受体激活后对柔红霉素血管内皮细胞毒性的保护作用,并探讨其保护机制。方法:EDU增殖实验检测内皮细胞的腺苷A3受体激动剂IB-MECA对内皮细胞增殖的影响;Western Blotting检测内皮细胞LC-3自噬蛋白表达的水平;Annexin V-FITC细胞凋亡检测试剂盒检测内皮细胞凋亡的情况。结果:柔红霉素抑制内皮细胞的增殖,诱导内皮细胞的凋亡和自噬性死亡,而IB-MECA则可以扭转柔红霉素的毒性,促进内皮细胞的增殖,降低内皮细胞的凋亡和自噬性死亡。结论:腺苷A3受体激活可以发挥对柔红霉素血管内皮细胞毒性的保护作用,为腺苷A3受体靶向药物与柔红霉素的联合化疗提供理论基础。Objective：To study activation of adenosine A3 receptor protecting vascular endothelial cells from daunomycin toxicity and its protection mechanism. Method： EDU cell proliferation assay was used to detect the effects of adenosine A3 receptor agonist IB-MECA on endothelial cell proliferation;We used western blotting to determine endothelial cells autophagy levels and Annexin V-FITC apoptosis detection kit to detect endothelial cell apoptosis case. Result： Daunorubicin inhibited endothelial cell proliferation and induce apoptosis and autophagic cell death in endothelial cells;The IB-MECA can reverse the toxicity of daunorubicin, promote the proliferation of en- dothelial cells,and reduced endothelial cell apoptosis and autophagic cell death. Conclusion： Adenosine A3 receptor activation may play a protective role for endothelial cells daunorubicin toxicity. Our results provides new methods for adenosine A3 receptor targeted drug in combination with daunorubicin chemotherapy.

关 键 词：腺苷A3受体 柔红霉素 内皮细胞 细胞死亡 

分 类 号：R733.710.5[医药卫生—肿瘤]