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目的 :研究芹菜素对肺癌A549/DDP细胞的作用,探讨芹菜素逆转肺癌耐药的作用及机制。方法 :体外培养肿瘤细胞,以不同浓度芹菜素作用为实验组,用MTT法检测A549/DDP细胞增殖和分析药物敏感性,用Rhodamine-123潴留实验检测A549/DDP细胞内药物外排情况,用Western blot法检测肿瘤细胞内P-糖蛋白(P-glycoprotein,P-gp)和肺耐药蛋白(lung resistance-related protein,LRP)表达情况,用RT-PCR法检测肿瘤细胞内多药耐药基因(multidrug resistance gene l,MDR1)m RNA和LRP m RNA的转录情况。结果 :与DDP组相比,20、40、80μmol/L的芹菜素明显抑制了A549/DDP细胞生长增殖(P<0.05)。DDP对A549/DDP细胞的IC50为(14.33±0.41)μg/m L,在芹菜素作用下其IC50降为(5.76±0.36)μg/m L,逆转倍数为2.48,两者相比有统计学差异(P<0.05)。芹菜素作用下,A549/DDP细胞内的Rhodamine-123蓄积增加,细胞内P-gp表达减弱,MDR1 m RNA转录水平下降,对LRP表达及LRP m RNA转录无明显改变。结论:芹菜素对A549/DDP细胞生长有抑制作用;芹菜素还具有逆转A549/DDP细胞肿瘤耐药的功能,其机制与降低MDR1 m RNA转录和下调P-gp介导的药物外转功能有关。
Objective: To study the effect of apigenin on lung cancer A549 / DDP cells and explore the effect and mechanism of apigenin on reversing lung cancer drug resistance. Methods: Tumor cells were cultured in vitro. The effects of different concentrations of apigenin were studied. The proliferation of A549 / DDP cells was assayed by MTT assay and the drug sensitivity was analyzed. Rhodamine-123 retention test was used to detect the drug efflux in A549 / DDP cells. Western blot was used to detect the expression of P-glycoprotein (P-gp) and lung resistance-related protein (LRP) in tumor cells. RT- (Multidrug resistance gene 1, MDR1) m RNA and LRP m RNA transcripts. Results: Compared with DDP group, apigenin of 20, 40 and 80μmol / L significantly inhibited the proliferation of A549 / DDP cells (P <0.05). The IC50 of DDP on A549 / DDP cells was (14.33 ± 0.41) μg / m L and its IC50 was (5.76 ± 0.36) μg / m L and the reversal multiple was 2.48 under the action of apigenin Difference (P <0.05). Under the action of apigenin, the accumulation of Rhodamine-123 in A549 / DDP cells increased, the expression of P-gp in cells decreased, the transcription level of MDR1 m RNA decreased, and there was no significant change in LRP expression and LRP m RNA transcription. Conclusion: Apigenin can inhibit the growth of A549 / DDP cells. Apigenin can also reverse the drug resistance of A549 / DDP cells. Its mechanism is related to the decrease of MDR1 m RNA transcription and the down-regulation of P-gp mediated drug transfer function .