摘要
目的观察蜂毒素对内皮祖细胞微血管形成的影响及探讨其作用机制。方法通过MTT比色法、黏附实验、Transwell小室迁移实验、小管形成实验等分别测定蜂毒素对内皮祖细胞的增殖、黏附、迁移、小管形成能力的影响。并且通过Western blot法测定蜂毒素对内皮祖细胞VEGFR1、VEGFR2、AKT、ERK1/2磷酸化的影响。结果随着蜂毒素的作用浓度增大,其对内皮祖细胞增殖的抑制力越强,蜂毒素浓度在2μg/ml以下时,不表现出明显的细胞毒性;与0μg/ml组相比较,蜂毒素1和2μg/ml浓度组对内皮祖细胞黏附、迁移和小管形成具有明显的抑制作用(P﹤0.05);蜂毒素可抑制内皮祖细胞磷酸化作用,并且下调VEGFR2的表达,VEGFR1的表达无明显变化。结论蜂毒素能明显抑制大鼠骨髓来源的内皮祖细胞的增殖、黏附、迁移、小管形成的能力,其作用机制可能与蜂毒素抑制内皮祖细胞的磷酸化信号转导通路,从而下调VEGFR2蛋白表达。
Objective To observe the effect of melittin on angiogenesis and discuse the mechanisms. Methods The proliferation, adhesion, migration, tube formation ability of endothelial progenitor cells(EPCs) were detected.Using MTT colorimetric method, adhesion experiment, Transwell cell migration experiment,tube formation experiment,respectively. Through the Western blot method, VEGFR1, VEGFR2, AKT, ERK1/2 phosphorylation expression of EPCs were determined.Results As the role of melittin concentration increases, proliferation of EPCs is stronger inhibited.When melittin concentration is below(including) 2 μg/ml, it does not show obvious cytotoxicity.The 1 and 2 μg/ml concentration groups of Melittin have obvious inhibitory effect on adhesion, migration and tubular formation of EPCs(P﹤0.05) vs. 0 μg/ml group.Melittin can obviously inhibit phosphorylation in EPCs and reduce VEGFR2 expression, but VEGFR1 expression had no obvious change.Conclusion Melittin can obviously inhibit proliferation, adhesion, migration and tube formation of EPCs. Mechanisms may be that Melittin inhibits phosphorylation of signal transduction pathway in EPCs, thereby VEGFR2 protein expression is down-regulated.
出处
《肿瘤防治研究》
CAS
CSCD
北大核心
2014年第4期289-293,共5页
Cancer Research on Prevention and Treatment
基金
国家自然科学基金面上项目资助(30873275)
关键词
蜂毒素
内皮祖细胞
血管内皮生长因子受体2
磷酸化
血管生成
Melittin
Endothelial progenitor cells(EPCs)
Vascular endothelial growth factor receptor 2(VEGFR2)
Phosphorylation
Angiogenesis
