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目的 :探讨 P- gp、bcl- 2蛋白在人红白血病多药耐药中的作用。方法 :用 MTT法、原位末端转移酶标记法、流式细胞术等分别对蝎毒诱导人红白血病耐药细胞株 (K5 6 2 / ADM)及敏感细胞株 (K5 6 2 )凋亡及其 P- gp、bcl- 2蛋白表达进行研究。结果 :蝎毒可明显抑制 K5 6 2及 K5 6 2 / ADM细胞生长和诱导细胞凋亡 (P<0 .0 5 ,P<0 .0 1) ,其作用强度在一定范围内呈现对浓度的依赖性 ;耐药细胞株中 P- gp、bcl- 2蛋白表达明显强于敏感细胞株 ;蝎毒可抑制 K5 6 2 / ADM细胞中 P- gp、bcl- 2蛋白表达。结论 :凋亡抑制基因 bcl- 2编码蛋白的过度表达可能是人红白血病多药耐药细胞凋亡耐受的分子基础 ,细胞凋亡与肿瘤细胞的耐药密切相关。
Objective: To investigate the role of P-gp, bcl-2 in multidrug resistance of human erythroleukemia. Methods: Apoptosis of K562 / ADM and K562 cells induced by scorpion venom were detected by MTT, in situ telomerase and flow cytometry, respectively. P-gp, bcl-2 protein expression was studied. Results: Scorpion venom could significantly inhibit the growth of K562 and K562 / ADM cells and induce apoptosis (P <0.05, P <0.01), and the intensity of scorpion venom showed a dose-dependent Dependent. The expression of P-gp and bcl-2 in drug-resistant cell lines was stronger than that in sensitive cell lines. Scorpion venom could inhibit the expression of P-gp and bcl-2 in K562 / ADM cells. Conclusion: Overexpression of bcl-2 protein may be the molecular basis of multidrug resistance in human erythroleukemia cells. Apoptosis is closely related to drug resistance of tumor cells.