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机构地区:[1]中国医学科学院医药生物技术研究所肿瘤室,北京100050
出 处:《中华医学杂志》2009年第25期1736-1740,共5页National Medical Journal of China
基 金:国家高技术研究发展计划基金(2006AA02A255)
摘 要:目的评价烯二炔类抗生素力达霉素对神经胶质瘤细胞血管生成拟态的抑制作用及对细胞凋亡的影响。方法C6和U87细胞凋亡以Annexin V-FITC/PI法结合流式细胞仪法进行分析,小管形成实验分析药物对神经胶质瘤细胞血管拟态的影响。结果0.1nmol/L(12.7±0.6)、0.5nmol/L(9.0±1.7)和1nmol/L(4.7±0.6)力达霉素处理的C6细胞血管生成拟态与对照(16.7±1.5)相比,差异有统计学意义(分别为P=0.013、P=0.005及P=0.0002);同样浓度的药物对U87细胞的血管生成拟态与对照(14.7±1.2)相比,差异有统计学意义(分别为P:0.025、P=0.005及P=0.0009)。相同剂量的力达霉素处理C6和U87细胞后其凋亡率与相应对照组相比差异有统计学意义。力达霉素对神经胶质瘤细胞血管生成拟态和细胞凋亡的影响明显比新制癌菌素强。结论力达霉素能够抑制神经胶质瘤细胞血管生成拟态并促进神经胶质瘤细胞凋亡,烯二炔类抗肿瘤抗生素治疗神经胶质瘤的研究值得进一步探讨。Objective To evaluate the in vitro effects of lidamycin upon vasculogenic mimicry and apoptosis induction in glioma ceils. Methods Tube formation assay was performed to estimate the inhibitory effects of lidamycin upon vasculogenic mimicry in C6 and U87 glioma cells. The vasculogenic mimicry of glioma cells was photographed and enumerated. Annexin V-FITC/PI was used for determination of glioma cell apoptosis with flow cytometry. Results Vasculogenic mimicry assay indicated that 0. 1 nmol/L, 0. 5 nmol/L and 1 nmol/L lidamycin showed significant inhibition of vasculogenic mimicry in C6 and U87 cells. Comparing with C6 control group (14.7±1.2), 0. 1 nmol/L (12.7±0.6), 0.5 nmol/L (9.0±1.7) and I nmol/L (4. 7±0. 6 ) lidamycin inhibited vasculogenic mimicry in C6 cells with statistical significances (P = 0. 013, P = O. 005 and P = 0. 0002 respectively). Comparing with U87 control group (14.7±1.2), the vasculogenic mimicry of 0.1 nmol/L (10.0±2.0), 0.5 nmol/L (8.3±1.5) and 1 nmol/L lidamycin (4. 3±0. 6) treated U87 cells showed statistical significances (P =0. 025, P =0. 005 and P =0. 0009 respectively). The apoptotic ratios of same dosages lidamycin treated C6 cells and U87 cells showed a similar tendency as vasculogenic mimicry inhibition (P 〈0.001 ). Lidamycin was more potent than neocarzinostatin in vasculogenic mimicry inhibition and apoptosis induction of C6 cells and U87 cells. Conclusion Lidamycin can inhibit vasculogenie mimicry and promote apotosis of glioma cells. Thus it is a promising drug in glioma treatment. Further researches on the therapeutic efficacy of enediyne antibiotics in glioma are needed.
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