a02
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K562 , K562 / A02 and clinic sample were used in the study .
蛋白质芯片检测多药耐药蛋白,是以细胞株(K562和K562/A02)、汉防己甲素和屈洛昔芬单独或联合作用的K562/A02耐药细胞及部分临床样品为实验研究对象。
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Study on reversal effects of Oridonin on multidrug resistant cell line K562 / A02
冬凌草甲素逆转多药耐药细胞系K562/A02耐药性的研究
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PSC 833 could increase DNR retention in K562 / A02 cells .
PSC833能增加K562/A02耐药细胞系的DNR潴留。
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The cell growth inhibition of K5662 / A02 cells was assayed using MTT method .
实验方法:K562/A02耐药性以MTT法检测阿霉素抑制细胞生长作用,计算耐药倍数。
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The Effect of Three Anthracycline Antineoplastic Drugs on K562 / A02 Cell Line Proliferation in vitro
三种蒽环类抗肿瘤药物对K562/A02细胞体外抑制作用
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Establishment and Evaluation of a Model using K562 / A02 Multidrug Resistant Tumor Xenografts in Nude Mice
多药耐药细胞系K562/A02裸小鼠皮下移植瘤模型的建立与鉴定
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Study of the effect of quercetin on expression of multidrug resistant gene and protein in K562 / A02 cells
槲皮素对K562/A02细胞多药耐药基因及糖蛋白表达的影响
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Effect of Intracellular Acidification on P-glycoprotein in Drug-resistant K562 / A02 Cells
细胞酸化对K562/A02耐药细胞株中P-糖蛋白的影响
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Study on Effect of Momordin on Reversion of Multidrug Resistance in K562 / A02 Cells
苦瓜蛋白对K562/A02耐药逆转作用的研究
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Reversal effect of artesunate on the multidrug-resistance of human leukemia K562 / A02 cells
青蒿琥酯逆转K562/A02细胞对阿霉素耐药性机理的研究
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Mechanism of tetrandrine in reversion of multidrug resistance of leukemic cell line K562 / A02
汉防己甲素逆转白血病细胞株K562/A02耐药的机制
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Effect of 4 cytokines on intracellular accumulation of daunorubicin in K562 / A02
4种细胞因子对K562/S及其耐药细胞株K562/A02积蓄柔红霉素的影响
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Study on reversal of drug resistance in K562 / A02 cells by antisense oligodeoxynucleotide targeting survivin
Survivin反义寡核苷酸逆转K562/A02细胞的耐药研究
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Primary observation of reversal of multidrug resistance in K562 / A02 cells with Radix Angelicae sinensis
当归药物血清逆转K562/A02细胞对阿霉素耐药性的初步观察
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CONCLUSION : Lomerizine could reverse the MDR in K562 / A02 cells by increasing the intracellular drug concentration .
结论:洛美利嗪对K562/A02细胞的ADM、VCR细胞毒性有剂量相关性增敏作用,其机制可能与增加细胞内药物浓度有关。
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Moreover , the expression of MAGE-3 gene mRNA in K562 / A02 cells was higher than that in K562 cells .
此外,与K562细胞比较,K562/A02细胞MAGE3mRNA表达明显上调。
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Functional study of mdrl and GST π expression reversed by hairpin siRNA in K562 / A02 cell line
发夹状siRNA逆转白血病K562/A02细胞株mdr1和GSTπ功能的研究
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Effect of Tetrandrine Combined with Daunorubicin on Expressions of P21 and P-gp in K562 / A02 Cells
汉防己甲素联合柔红霉素对K562/A02细胞株P21蛋白和P糖蛋白表达的影响
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Objective : To compare the effect of three kinds of anthracycline antineoplastic drugs on K562 / A02 cell line proliferation in vitro .
目的:比较表阿霉素,柔红霉素和吡喃阿霉素对多药耐药细胞株K562/A02体外增殖的抑制作用。
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Study on the Relationship Between [ Ca ~ ( 2 + ) ] I and the MDR Formation in K562 / A02 Cells
细胞内钙与K562/A02细胞多药耐药相关性的研究
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Enhancement of cytotoxicity of anthracycline antineoplastic drugs by neferine in K562 / A02 cells
甲基莲心碱增强蒽环类药物对K562/A02细胞增殖抑制作用实验研究
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Objective To study the effect of thapsigargin on chemotherapeutic sensitivity in multidrug-resistant leukemia cell line K562 / A02 induced by ADM.
目的探讨内质网Ca2+ATP酶抑制剂thapsigargin对白血病多药耐药细胞株K562/A02化疗敏感性的影响。
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Conclusions Antisense oligonucleotides complementary to CYP3A5 gene may obviously reverse the drug-resistant phenotype of K562 / A02 cells .
结论:针对CYP3A5基因的反义寡核苷酸可显著逆转K562/A02细胞的耐药性。
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Apoptosis of Multidrug-resistant Human Leukemia Cell Line K562 / A02 Induced by Fraction C ⅱ from Naja Naja Actra Venom
中华眼镜蛇毒组分CⅡ诱导多药耐药白血病细胞K562/A02凋亡
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Decrease of cellular GSH concentration may be one of the MDR reversal mechanisms in K562 / A02 cell line by neferine and erythromycin .
结论:细胞内GSH含量增高是K562/A02细胞产生MDR的机制之一;Nef,EM能使K562/A02细胞内GSH含量下降可能是其逆转耐药白血病细胞MDR的机制之一。
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Morphological change of K562 / A02 cells treated with thapsigargin was examined with AO / EB fluorescent staining under fluorescent microscopy .
丫啶橙(AO)/溴化乙锭(EB)染色荧光显微镜观察thapsigargin处理后K562/A02细胞形态改变;
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Objective To study the molecular mechanism underlying multidrug resistance ( MDR ) and identify unknown genes that might be involved in drug resistance development in K562 / A02 cells .
目的分析K562/A02细胞多药耐药性(MDR)分子机制,寻找可能参与K562/A02细胞耐药机制的新基因。
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In conclusion , the mechanism of Tet and DRL reversing multidrug resistance has no correlation with the apoptosis of K562 / A02 cells .
结论:汉防己甲素,屈洛昔芬逆转耐药的机理与诱导K562A02细胞凋亡无关。
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50 % inhibition concentration ( IC_ 50 ) of doxorubicin ( ADM ) for K562 / A02 cell line was determined by MTT method .
MTT法检测阿霉素对K562/A02细胞半数抑制浓度(IC50)。
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Methods : After treatment with TNF - α and IFN - α respectively , K562 / A02 sensitivity to ADR was investigated using tetrazolium dye assay .
方法:应用MTT法,分析TNFα和IFNα(均为100U/ml)分别处理K562/A02前后,K562/A02对ADR敏感性的变化。