EGCG对多发性骨髓瘤细胞KM3促血管新生作用的抑制效应及机制初探.docVIP

EGCG对多发性骨髓瘤细胞KM3促血管新生作用的抑制效应及机制初探 【摘要】??本研究探讨绿茶茶多酚成分之一表没食子儿茶素没食子酸酯［(－)epigallocatechin3gallate，EGCG)?］对多发性骨髓瘤细胞KM3促血管新生作用的影响及其机制。?体外培养多发性骨髓瘤细胞KM3，观察不同浓度EGCG作用后的培养上清对血管内皮细胞株HUVEC迁移和形成血管能力的影响。ELISA法检测KM3细胞培养上清中血管内皮生长因子（VEGF）分泌水平；RTPCR方法检测KM3细胞VEGF?mRNA表达水平。?结果表明：?EGCG以浓度依赖方式抑制KM3细胞培养上清促内皮细胞迁移的作用，5,?25,?50和100?μmol/L的EGCG迁移细胞数目分别为414±27，299±70，202±42及?116±13个，且EGCG的浓度与内皮细胞的迁移数目呈负相关（r=?-0.952,p0.05）。同时，内皮细胞形成小管的面积随EGCG浓度的升高而减少，?25及50?μmol/L时的面积分别是88343.9±3231.1和60897.5±914.1?μm2，均明显低于对照组（p＜0.01)，小管面积与EGCG浓度呈负相关（r=?-0.888,p0.05）。5、25、50、100?μmol/L的EGCG作用于KM3细胞48小时后培养上清中VEGF的含量分别为1399.0±47.4?pg/ml，660.1?±5.7?pg/ml，108.5?±5.8?pg/ml和26.2±18.6?pg/ml，与对照组比较，25、50、100?μmol/L组均有统计学意义（p＜0.01）。RTPCR结果显示EGCG抑制KM3细胞VEGF的?mRNA水平表达，且呈浓度依赖性。结论：?EGCG能显著抑制多发性骨髓瘤细胞KM3的促血管新生作用；下调VEGF转录水平的表达，减少VEGF的分泌可能是其药理作用机制之一。?医学论文网【关键词】??多发性骨髓瘤????Inhibitory?Effect?of??EGCG?on?Angiogenesis?Induced?by?Multiple?Myeloma?Cell?line?KM3?and?Its?Mechanism????SHAO?Jing,?CHEN?ZhiChao,?LI?QiuBai,?L?Jian????Institute?of?Hematology?,?Union?Hospital?,?Tongji?Medical?College?,?Huazhong?University?of?Science?and?Technology?,?Wuhan?430022?,?China????Abstract????The?aim?of?this?study?was?to?investigate?the?effect?of??［(-)epigallocatechin3gallate??(EGCG)］?on?angiogenesis?induced?by?multiple?myeloma?cell?line?KM3?and?its?mechanism.??The??effects?of?KM3?cell?supernatant?after??being??treated??with?EGCG?in?different?concentrations?on?migration?and?vascular??formatiem?ability?of?endothelial?cell?line?HUVEC?were?investigated?through?culture?of?MM?cell?line?KM3?in?vitro.??The?secretion??level?of?vascular?endothelial?growth?factor?(VEGF)?in?KM3?cell?supernatant?and?the?expression?level?of?VEGF?mRNA?in?KM3?were?detected?by?ELISA?and?RTPCR?respectively.??The?results?indicated?that?the?KM3?cell?supernatant?significantly?induced?endothelial?cell?migration?and?vassel?formation?in?vitro.?EGCG?inhibited?the?effect?of?endothelial?cell?migration?induced?by?KM3?cell?supernatant,?and?the?numbers?of?migrated?cells?w