油茶皂苷对脂多糖诱导人脐静脉内皮细胞ICAM-1表达的抑制作用

 目的观察油茶皂苷(SQS)对脂多糖(LPS)诱导人脐静脉内皮细胞(HUVECs)ICAM-1表达的作用并探讨其作用机制。方法建立HUVECs LPS应激模型,以油茶皂苷(10.0,1.0,0.1μmol·L^-1)和ERK1/2抑制剂PD98059(10.0μg·L^-1)预处理细胞8h,取培养细胞上清液测定LDH活性,HUVECs分别用于测定细胞存活率及ICAM-1 mRNA和蛋白的表达。结果LPS可显著升高LDH活性,上调ICAM-1 mRNA和蛋白的表达(P<0.01)。SQS呈浓度依赖性地对抗上述改变,其作用与PD98059的作用相似。结论SQS可抑制LPS诱导的HUVECs ICAM-1表达的上调,其机制可能与MAPK-ERK1/2(MEK1/2)信号转导通路有关。

Inhibitory Effects of Sasanquasaponin on ICAM-1 Over-Expression Induced by Lipopolysaccharides in Human Umbilical Vein Endothelial Cells

OBJECTIVE To study the effects of sasanquasaponin(SQS)on intercellular adhesion molecule-1(ICAM-1) over-expression induced by lipopolysaccharides(LPS) in human umbilical vein endothelial cells(HUVECs) and its possible mechanisms.METHODS HUVECs were exposed to SQS(10.0,1.0,0.1 μmol·L^-1) or/and PD98059(10.0 μg·L^-1),an inhibitor of extracellular-signal regulated kinase(ERK1/2),for 8 h in LPS-stress model.Lactate dehydrogenase(LDH) activity in the HUVECs supernatants was determined.The resulting HUVECs viability was measured spectrophotometrically and the expression of ICAM-1 mRNA and its protein was assayed by RT-PCR and Western blots,respectively.RESULTS The elevations of LDH activity and ICAM-1 expression levels were observed in LPS-stress group,and there were significant differences compared with control group(P<0.01)Inversely,SQS antagonized these changes in a concentration-dependent manner and the inhibitory effect of SQS resembled that of PD98059.CONCLUSION SQS inhibites the over-expression of ICAM-1 induced by LPS-stress and its mechanism is possibly related to MAPK-ERK1/2 signal pathway.