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目的：阐明Ａｓ２Ｏ３诱导Ｋ５６２细胞凋亡的可能机制，为Ａｓ２Ｏ３治疗白血病的推广应用提供一定的理论基础。方法：采用免疫沉淀、Ｗｅｓｔｅｒｎｂｌｏｔ及生物化学等方法，观察在Ａｓ２Ｏ３诱导Ｋ５６２细胞凋亡过程中，细胞胞浆和胞膜蛋白及ＡＢＬ蛋白酪氨酸激酶（ＰＴＫ）活性及某些内源性蛋白酪氨酸磷酸化的变化。结果：在Ａｓ２Ｏ３诱导Ｋ５６２细胞凋亡过程中，细胞胞浆和胞膜蛋白及ＡＢＬ蛋白ＰＴＫ活性降低，分子量为１８万和１２．５万的蛋白酪氨酸磷酸化减少。结论：Ａｓ２Ｏ３可能通过降低细胞内某些蛋白，尤其ＢＣＲ／ＡＢＬ蛋白的ＰＴＫ活性，减少蛋白酪氨酸磷酸化，从而阻断ＢＣＲ／ＡＢＬ抗凋亡信号的传导，诱导Ｋ５６２细胞凋亡
OBJECTIVE: To elucidate the possible mechanism of apoptosis induced by As2O3 in K562 cells and to provide a theoretical basis for its application in the treatment of leukemia. Methods: Immunocytochemistry, Westernblot and biochemistry were used to observe the cytosolic and cytoplasmic membrane proteins and the activity of ABL protein tyrosine kinase (PTK) in As2O3-induced K562 cells and the effects of some endogenous proteins Amino acid phosphorylation changes. Results: During As2O3-induced K562 cell apoptosis, cytosolic and cytoplasmic membrane proteins and ABL protein PTK activities were decreased. The phosphorylation of tyrosine phosphates with molecular weights of 180,000 and 125,000 were decreased. CONCLUSION: As2O3 may decrease the tyrosine phosphorylation of certain proteins in the cell, especially the BCR / ABL protein, thereby blocking the transduction of BCR / ABL anti-apoptotic signal and inducing the apoptosis of K562 cell