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作 者:郭健欣[1] 周雅虹[2] 潘敬新[1] 郭熙哲[1] 黄月琴[1] 郭雅斐 GUO Jian-Xin;ZHOU Ya-Hong;PAN Jng-Xin;GUO Xi-Zhe;HUANG Yue-Qin;GUO Ya-Fei(Department of Hematology,The Second Affiliated Hospital of Fujian Medical University,Quanzhoo 362000,Fujian Province,China;Department of Hemodialysis,The Second Affiliated Hospital of Fujian Medical University,Quanzhoo 362000,Fujian Province,China)
机构地区:[1]福建医科大学附属第二医院血液内科,福建泉州362000 [2]福建医科大学附属第二医院血液透析室,福建泉州362000
出 处:《中国实验血液学杂志》2018年第5期1360-1365,共6页Journal of Experimental Hematology
摘 要:目的:探讨苯丁酸氮芥对B细胞淋巴瘤细胞株A20细胞是否具有促凋亡效应及其在凋亡信号通路中的具体作用机制。方法:实验组使用终浓度为20μmol/L的苯丁酸氮芥处理A20细胞,对照组使用PBS处理A20细胞。使用Annexin V-FITC细胞凋亡检测试剂盒检测细胞的凋亡情况,使用Western blot检测淋巴瘤细胞中Active caspase-3、Survivin、NF-κB和p AKT的表达,使用荧光定量PCR检测淋巴瘤细胞中Survivin mRNA的表达。结果:与对照组相比较,苯丁酸氮芥干预组的A20细胞FITC^+/PI^+凋亡细胞的比例显著增高,而Active caspase-3的表达显著上调(t=7. 384,P=0. 000),Survivin mRNA的表达显著降低(t=4. 384,P=0. 000),Survivin蛋白的表达显著降低(t=12. 360,P=0. 000),NF-κB蛋白的表达显著降低(t=5. 462,P=0. 000),p AKT的表达显著降低(t=7. 183,P=0. 000)。结论:苯丁酸氮芥促进淋巴瘤细胞凋亡,其机制可能与抑制PI3K/AKT信号通路、NF-κB和Survivin的表达有关。Objective:To study whether chlorambucil has apoptotic effect on the B cell lymphoma A20 cells and its exact mechanisms in apoptotic signaling pathway.Methods:The experimental cells were treated with 20 pmol/L chlorambucil,the control cells were treated with PBS.Annexin V-FITC Cell Apoptosis Detection Kit was used to examine cell apoptosis.Western blot was used to detect the expressions of active caspase-3,Survivin,NF-KB and pAKT.Real-time fluorescent quantitative PCR was performed to examine the mRNA expression of Survivin.Results:Compared with the control group,the proportion of FITC+/PI+apoptotic cells and the expression of active caspase-3(t=7.384,P=0.000)in the chlorambucil treatment group was significantly elevated.However,the expression of Survivin mRNA(/=4.384,P=0.000),protein expressions of survivin(t=12.360,P=0.000),NF-KB(/=5.462,P=0.000)and pAKT(t=7.183,P=0.000)in the chlorambucil-treated group all significantly decreased.Conclusion:The chlorambucil can induce the apoptosis of lymphoma cells,its mechanism may related with inhibition of PBI^AKT signaling pathway,and expression of NF-KB and survivin.
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