去甲斑蝥素对多发性骨髓瘤细胞周期和血管内皮细胞生长因子的影响  

Effect of norcantharidin on vascular endothelial growth factor and cell cycle of general lymphadenomatosis of bones

作　　者：杜恒飞[1] 于路佳[1] 郝京生 胡晓东 吕鸿雁[1] 李娜 张金巧[1] 

机构地区：[1]河北医科大学第三医院,石家庄050051 [2]石家庄肾病医院肿瘤免疫治疗研究中心 [3]临城县人民医院

出　　处：《山东医药》2012年第1期22-24,共3页Shandong Medical Journal

基　　金：河北省中医药管理局科研课题(2007136)

摘　　要：目的探讨去甲斑蝥素(NCTD)抗骨髓瘤效应的机制。方法利用流式细胞术检测不同浓度NCTD作用24 h后细胞周期的改变,Western blot检测CDK1、cyclin A和cyclin B1的改变,免疫组化和RT-PCR测定血管内皮细胞生长因子(VEGF)的表达。结果经NCTD处理24 h后,随着NCTD浓度增加,G2/M期细胞明显增加,S期细胞明显减少,呈剂量依赖性;NCTD以剂量依赖的方式抑制cyclin B1、CDK1和cyclin A的表达;NCTD以剂量依赖的方式抑制VEGF mRNA和蛋白的表达。结论 NCTD对U266细胞有抗增殖和促凋亡作用,其作用机制可能与调节细胞周期和抑制VEGF的表达有关。To explore the anti-myeloma effect of norcantharidin （NCTD） and the possible mechanism. Methods U266 cells were treated with 0, 5, 10 and 20 μmol/L NCTD for 24 h. Flow cytometry was used to determine cell cycle distribution. The protein expressions of CDK1, cyclin A and cyclin B1 were determined by Western blot. RTPCR and immunohistochemistry were used to determine the expression of vascular endothelial growth factor（VEGF）. Resuits U266 cells were markedly arrested at G2/M phase after treatment with different concentration of NCTD after 24 hours, while the cells in S phase decreased from （51.53 ± 6.9） % to （ 17.6 ± 1.3 ） % ; NCTD inhibited the protein expressions of cyclin B1, CDK1 and cyclin A in dosedependent manner（ P 〈 0.05 ） ; the protein and mRNA expressions of VEGF were downregulated in dosedependent manner（ P 〈 0.05 ）. Conclusions NCTD displays potent antiproliferative activity through suppressing cell cycle proteins, arresting cell cycle at G2/M phase and inhibiting the expression of VEGF.

关 键 词：多发性骨髓瘤 去甲斑蝥素 细胞周期 血管生成 

分 类 号：R733.3[医药卫生—肿瘤]