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目的 :观察 Raji细胞抵抗阿霉素诱导细胞凋亡的分子机制 ,从细胞凋亡的角度探讨肿瘤细胞耐药机制。方法 :MTT方法测定阿霉素和肽素诱导的细胞毒实验 ,碘化丙啶染色 FACS和 DNA降解断裂法分析阿霉素诱导的细胞凋亡 ,FACS分析 Raji细胞 bcl- 2的表达 ,Western bolt观察 Raji细胞 p5 3、bax分子的表达 ,RT- PCR检测 MDR1、MRP和 GSTπ的表达水平。结果 :Raji细胞对阿霉素和肽素均产生明显药物耐受 ,同时抵抗药物诱导的细胞凋亡 ;Raji细胞中 bcl- 2分子呈诱导性表达 ,不表达或弱表达 bax、p5 3分子 ;Raji细胞组成性高表达 MDR1、MRP、GSTπ等耐药相关分子。结论 :Raji细胞抵抗药物诱导的细胞凋亡是化疗耐受的重要原因。其中细胞膜表面分子 MDR1、MRP的高表达 ,细胞质中 bcl- 2诱导性高表达 ,bax、p5 3分子的弱表达是导致药物耐受和抵抗细胞凋亡的重要因素。
Objective: To observe the molecular mechanism of Raji cells against apoptosis induced by doxorubicin, and to explore the mechanism of drug resistance in tumor cells from the perspective of apoptosis. METHODS: MTT assay was used to determine the doxorubicin- and copeptin-induced cytotoxicity assay. Propidium iodide stained FACS and DNA degradation was used to analyze doxorubicin-induced apoptosis. FACS analysis of bcl-2 expression in Raji cells was performed. Western blot The expression of p53 and bax molecules in Raji cells was observed, and the expression levels of MDR1, MRP, and GSTπ were detected by RT-PCR. RESULTS: Raji cells produced significant drug resistance to both adriamycin and copeptin, while resisting drug-induced apoptosis; bcl-2 molecules in Raji cells showed inducible expression, and did not express or weakly express bax, p53 molecules; Raji cell constitutively expresses MDR1, MRP, GSTπ and other drug-resistance related molecules. Conclusion : Raji cell resistance to drug-induced apoptosis is an important reason for resistance to chemotherapy. The high expression of MDR1 and MRP molecules on the surface of the cell membrane and the high expression of bcl-2 in the cytoplasm, weak expression of bax and p53 molecules are important factors leading to drug tolerance and resistance to apoptosis.