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红霉素预适应诱发胶质瘤耐药作用机制探讨

Mechanism of BCNU resistance in glioma cells induced by erythromycin preconditioning
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摘要 目的探讨红霉素预适应对胶质瘤细胞系U251对亚硝基脲类药物BCNU耐药的影响及其可能的机制。方法400mmol/L红霉素预处理U251细胞3h后以BCNU刺激细胞(预适应刺激组),同时设刺激组和空白对照组。应用MTT法和流式细胞技术分别检测细胞的增殖和凋亡率.RT—PCR方法检测U251细胞神经型一氧化氮合酶(nNOS)和Bcl-2 mRNA的表达情况。结果与刺激组相比,红霉素预适应刺激组细胞的增殖能力增加,凋亡率减少,差异有统计学意义(P〈0.05),RT-PCR结果显示nNOS、Bcl-2 mRNA的表达增加。结论红霉素预处理U251细胞可以增加其对BCNU的耐药作用,nNOS和Bcl-2可能参与了这一过程的调节。 Objective To explore the effect of erythromycin preconditioning on carmustine (BCNU) resistance in glioma cell line (5251 and its mechanism. Methods U251 cells was pretreated with 400 mmol/L erythromycin for 3 h followed by 30 μg/mL BCNU exposure. MTT assay and flow cytomertry were employed to detect the proliferation and apoptotic index of the cells in comparison with those of BCNU-treated U251 cells without erythromycin preconditioning and blank control cells. RT-PCR was used to detect the mRNA expressions of neuronal nitric oxide synthase (nNOS) and Bcl-2 genes in these cells. Results Compared with the BCNU treatment alone, erythromycin preconditioning prior to BCNU exposure resulted in significantly increased cell proliferation and decreased cell apoptosis (P〈0.05) and upregnlated the expressions of nNOS and Bcl-2 mRNAs. Conclusion Erythromycin pretreatment can induce BCNU resistance in U251 cells, and nNOS and Bcl-2 genes may play a regulatory role in this process.
出处 《中华神经医学杂志》 CAS CSCD 北大核心 2009年第10期990-992,共3页 Chinese Journal of Neuromedicine
基金 辽宁省科技攻关项目(2006401013-3) 辽宁省自然科学基金(20072099)
关键词 红霉素预适应 神经型一氧化氮合酶 细胞凋亡 Erythromycin preconditioning Neuronal nitric oxide synthase Apoptosis
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