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目的:观察康莱特对耐药细胞的作用及分子机制。方法:以敏感型乳腺癌细胞株 MCF7为对照,四氮唑蓝(MTT)法检测康莱特对耐药细胞株 MCF7~(adr)的抑制作用。以 Annexin V 标记法、DNA 含量测定法及电镜观察康莱特的诱导耐药细胞 MCF7~(adr)凋亡及周期阻滞的作用。免疫组化法检测康莱特对 MCF7~(adr)细胞 p53、p21~(WAF1/CIP1)蛋白表达的影响,RT-PCR 法检测康莱特对 MCF7~(adr)细胞 p21~(WAF1/CIP1)mRNA 表达水平的影响。结果:康莱特对 MCF7~(adr)细胞的半数抑制剂量(IC_(50))为26μ1/ml,与其对敏感细胞 MCF7的 IC_(50)(21μ1/ml)差异无显著性(P>0.05)。康莱特能诱导 MCF7~(adr)出细胞凋亡及细胞周期阻滞(G_0/G_1及 G_2/M 期),使 p53蛋白、p21~(WAF1/CIP1)mRNA 及蛋白表达水平升高。结论:康莱特对耐药细胞同样有效,这为其临床应用于已产生耐药性的肿瘤提供了依据。
Objective: To observe the effect and mechanism of KLT on drug-resistant cells. Methods: The MCF7 sensitive breast cancer cell line was used as the control and the tetrazolium blue (MTT) method was used to detect the inhibition of Kanglaite on MCF7 adr. Annexin V labeling, DNA content determination and electron microscopy were used to observe the apoptosis and cell cycle arrest of Kanglaite-induced MCF7 adr cells. The effect of KLT on the expression of p53, p21 WAF1/CIP1 protein in MCF7 adr cells was detected by immunohistochemistry. The p21 WAF1/CIP1 mRNA was detected by RT-PCR on MCF7 adr cells. The effect of expression levels. Results: The half inhibitor (IC 50 ) of Kanglaite on MCF 7 adr cells was 26 μ1/ml, and there was no significant difference between IC 50 and 21 μ 1 /ml of MCF 7 sensitive cells (P>0.05). . Kanglaite can induce MCF7 adr apoptosis and cell cycle arrest (G_0/G_1 and G_2/M phases), and increase the expression of p53 protein, p21 WAF1/CIP1 mRNA and protein. Conclusion: Kanglaite is equally effective for resistant cells, which provides a basis for its clinical application to tumors that have developed resistance.