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SELEX技术筛选人慢性粒细胞白血病(CML)核酸适配子,合成aptamer-si RNA核酸复合物,观察aptamer-si RNA核酸复合物干预NOD/SCID小鼠慢性粒细胞白血病(CML)bcr-abl融合基因及P210、P53、TNF-α、bcl-xl相关因子表达水平。将K562细胞接种于全身照射后的裸鼠,待皮下成瘤后取出瘤块,制备成瘤细胞混悬液,再尾静脉接种于NOD/SCID小鼠,实验成功建立了全身播散型白血病模型,对实验小鼠行随机分组,以RT-PCR法检测aptamer-si RNA核酸复合物治疗小鼠体内bcr-abl融合基因表达水平,ELASA法检测小鼠P210、P53、TNF-α、bcl-xl表达水平。实验结果表明:Aptamer-si RNA核酸复合物可显著降低模型小鼠体内融合基因bcr-abl及融合蛋白P210表达水平,能提升P53表达,抑制TNF-α、bcl-xl过度表达,其抑制效果与aptamer-si RNA核酸复合物浓度有一定的相关性。aptamer-si RNA核酸复合物通过干预CMLbcr-abl融合基因及其表达的融合蛋白P210,影响细胞信号传导通路途径,有效阻断了CML传变的进展,揭示了aptamer-si RNA核酸复合物干预CML疾病的微观机理。
SELEX technology screening of human chronic myeloid leukemia (CML) nucleic acid aptamers, synthesis aptamer-si RNA nucleic acid complex observed aptamer-si RNA nucleic acid complex interference NOD / SCID mouse CML bcr-abl fusion Gene and P210, P53, TNF-α, bcl-xl expression levels of related factors. The K562 cells were inoculated into nude mice after whole body irradiation and the tumor masses were removed after subcutaneous tumor formation to prepare tumor cell suspension. The tail vein was inoculated into NOD / SCID mice. The model of systemic disseminated leukemia The mice were randomized into groups. The expression of bcr-abl fusion gene in aptamer-si RNA complexes was detected by RT-PCR. The levels of P210, P53, TNF-α, bcl-xl The expression level. The results showed that Aptamer-si RNA complex could significantly decrease the expression of fusion gene bcr-abl and fusion protein P210 in model mice, increase the expression of P53 and inhibit the over-expression of TNF-α and bcl-xl, Aptamer-si RNA nucleic acid complex concentration has a certain correlation. The aptamer-si RNA nucleic acid complex can effectively block the progress of CML transformation by intervening the CMLbcr-abl fusion gene and its expression fusion protein P210, thereby affecting the cell signaling pathway and revealing that aptamer-si RNA complex interferes with CML Microscopic mechanism of disease.