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小檗碱抗肿瘤新生血管形成作用机制的研究 被引量:26

The study of the effect mechanism of berberine on anti-tumor angiogensis
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摘要 目的:研究小檗碱对bFGF活化人脐静脉内皮细胞(HUVEC)增殖、细胞周期及细胞凋亡的影响,探讨其对肿瘤新生血管形成作用的机制。方法:MTT法检测小檗碱对bFGF活化HUVEC的增殖作用;流式细胞仪检测用药后细胞周期的变化;激光共聚焦扫描显微镜下观察药物对细胞形态、细胞内钙的影响;流式细胞仪检测小檗碱对细胞凋亡的作用。结果:小檗碱能明显抑制bFGF活化的HUVEC增殖,且存在剂量依赖关系;使细胞在G0-G1期的比例明显增多;使细胞核浓缩、甚至裂解成碎块,同时使细胞内钙增多;并诱导活化HUVEC发生细胞凋亡。结论:小檗碱可能通过将bFGF活化的HUVEC细胞周期阻滞在G0-G1期,抑制活化HUVEC的增殖;诱导活化HUVEC细胞发生凋亡等机制,阻止新生血管形成,发挥其抗肿瘤作用。 Objective: To study the effect of berberine on cell proliferation, cell cycle and cell apoptosis in bFGF activated HUVEC. To investigate the mechanism of inhibitory tumor angiogenesis. Methods:MTT assay was used to determine the cell proliferation effect by berberine. The change of cell morphology and cell cycle was detected by laser scanning confocal microscope and flow cytometry, respectively. Flow cytometry was applied to detected the cell apoptosis rate. Results: The proliferation of HUVEC was inhibited by berbefine in a dose-dependent manner. The cell cycle were arrested in G0-G1. The cell nuclear condensation and nuclear cataclasm were found under laser scanning confocal microscope. Simultaneity increased intracellular calcium ion was observed after drug treatment. Berbefine induced activated HUVEC apoptosis. Conclusion:Berberine could inhibit tumor angiogenesis by arresting activated HUVEC in G0-G1, proliferation and apoptosis of tumor.
出处 《中国免疫学杂志》 CAS CSCD 北大核心 2006年第3期235-236,243,共3页 Chinese Journal of Immunology
关键词 小檗碱 HUVEC 细胞周期 凋亡 Berberine HUVEC Cell cycle Apoptosis
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