ECV304 was reported first in 1990 as a spont aneously-transformed and immortalized cell line derived from a Japanese HUVEC. S ubsequently, many studies validated that the ECV304 is a permanent endothelial cell line. I...ECV304 was reported first in 1990 as a spont aneously-transformed and immortalized cell line derived from a Japanese HUVEC. S ubsequently, many studies validated that the ECV304 is a permanent endothelial cell line. It has been used widely as an endothelial cell model and an useful re search tool in biomedicine and pharmacology. However, several distinct differenc es exist between ECV304 and HUVEC. Some studies even pointed out that ECV304 is not of HUVEC origin. According to the research data including ours, this reporte dly endothelial-derived permanent human cell line ECV304 may be dedifferentiated towards an epithelial phenotype. It is therefore not an appropriate cell line t o study endothelial cell biology. But cultured ECV304 cells can still be used as a model, tool or target in the pathophysiological and pharmacological studies, depending on whether or not their functional expression or markers are suitable for the research work.展开更多
文摘目的考察麦冬中主要皂苷元鲁斯可皂苷元(Rusco-gen in)抑制细胞黏附的作用,为深入研究其抗炎作用机制提供依据。方法采用MTT比色法检测Ruscogen in对人原髓性白血病细胞株HL-60细胞与正常或肿瘤坏死因子-α(TNF-α)活化的人脐静脉内皮细胞株ECV304细胞黏附的影响及其对ECV304与HL-60细胞增殖的影响。结果Ruscogen in 0.1,1.0μmol.L-1预处理ECV304细胞后,均抑制TNF-α诱导的ECV304细胞与HL-60细胞黏附的增加,Ruscogen in 0.001,0.01,0.1μmol.L-1预处理HL-60后,亦抑制TNF-α诱导的ECV304细胞与HL-60细胞黏附的增加;同时Ruscogen in在实验浓度范围内不影响ECV304细胞与HL-60细胞的增殖及二者之间的正常黏附。结论Ruscoge-n in可通过抑制HL-60细胞与活化的ECV304细胞之间的黏附作用,发挥抗炎活性。
文摘ECV304 was reported first in 1990 as a spont aneously-transformed and immortalized cell line derived from a Japanese HUVEC. S ubsequently, many studies validated that the ECV304 is a permanent endothelial cell line. It has been used widely as an endothelial cell model and an useful re search tool in biomedicine and pharmacology. However, several distinct differenc es exist between ECV304 and HUVEC. Some studies even pointed out that ECV304 is not of HUVEC origin. According to the research data including ours, this reporte dly endothelial-derived permanent human cell line ECV304 may be dedifferentiated towards an epithelial phenotype. It is therefore not an appropriate cell line t o study endothelial cell biology. But cultured ECV304 cells can still be used as a model, tool or target in the pathophysiological and pharmacological studies, depending on whether or not their functional expression or markers are suitable for the research work.
文摘目的研究丹参酮A(TAN A)对急性早幼粒细胞性白血病(APL)细胞株NB4诱导的人ECV304细胞株促凝活性的影响。方法1分别用0.5ΜG/ML TAN A、0.3ΜG/ML ATRA、0.1G/L DMSO、RPMI1640处理培养NB4细胞制成条件培养基TAN A-NB4-CM,ATRA-NB4-CM、DMSO-NB4-CM以及RPMI1640-NB4-CM,再分别与ECV304细胞在37℃共同孵育0、4、8、12H,利用复钙时间测定及改良发色底物法,分别测定ECV304细胞裂解液的肿瘤促凝活性(PCA)和组织因子活力(TF:ACT)。2ECV304细胞分别与0.5ΜG/ML TAN A及TAN A-NB4-CM在37℃共同孵育4、12、24、72、120H,用上述同样方法测定ECV304细胞裂解液的PCA和TF:ACT。结果10.5ΜG/ML TAN A处理NB4细胞24、72、120H的条件培养基能使ECV304细胞PCA增强,ATRA具有相似作用(P>0.05)。20.5ΜG/ML的TAN A对0.5ΜG/ML TAN A作用NB4120H的条件培养基(TAN A-120H-NB4-CM)促ECV304细胞PCA有抑制作用,其作用强度呈时间依赖性,120H达到高峰,再增加TAN A浓度,作用强度不增加;与0.3ΜG/ML ATRA作用相似。3TAN A-120H-NB4-CM能够增加ECV304细胞TF:ACT,并随作用时间增加而增强,TAN A与ATRA作用相似(P>0.05)。40.5ΜG/ML TAN A能够抑制TAN A-120H-NB4-CM对ECV304细胞的TF:ACT,并随作用时间增加而增强,ATRA具有相似作用(P>0.05)。结论TAN A在诱导NB4细胞分化凋亡的同时,可能通过某种因子增强NB4细胞对ECV304细胞促凝活性和组织因子活力;TAN A能够有效阻止NB4细胞增强ECV304细胞的促凝活性和组织因子活力,起到保护细胞的作用。
