β-细辛醚对Aβ痴呆损伤过程中ECV304细胞黏附分子表达的影响(英文)

Effect of β-asarone on expression of ECV340 cell adhesion molecules induced by β-amyloid peptide

目的:了解Alzheimer’s病中β-淀粉样蛋白沉积在血管内皮细胞给其造成的损伤,以及β-细辛醚对血管内皮细胞黏附分子表达的影响和对血管内皮细胞损伤修复的影响。方法:运用形态学、流式细胞术及MTT法,检测Aβ损伤、正常和β-细辛醚治疗的ECV304细胞的DNA周期,钙离子浓度及CD106,CD62P,CD62E这3种黏附分子表达的变化。结果:β-淀粉样蛋白在血管内皮细胞痴呆损伤过程中,上调其他3种黏性分子和钙离子浓度,造成细胞凋亡;β-细辛醚能下调3种黏性分子的表达和钙离子浓度,减少细胞凋亡。结论:β-细辛醚通过调节某些外周血小板黏附分子和血管间黏附分子和钙离子浓度,减轻β-淀粉样蛋白对血管内皮细胞的痴呆损伤。

AIM： To explore the effect of β-asarone on vascular endothelium and adhesion molecule expression of endothelium induced by β-amyloid peptide from Alzheimer＇s disease and to estimate the injury repair. METHODS： Cultured ECV304 cells were incubated with freshly solublized Aβ1-42 and the mixture of Aβ1.42 and β-asarone, the expression of three central adhesion molecules, CD106, CD62P, CE62E and Ca^2＋ concentration were examined and apoptosis was recorded by Flow cytometry. Test viability of cells by MTT methods. RESULTS ： The resuits showed that in model group and treated group, ligation of endothelial CD106, CD62P, CE62E, markers for endothelial cell activation and Ca^2＋ concentration, leads to a lot of release. The livability decreased and the apoptosis increased. Further more, simultaneous treatment of ECV304 cells with β-asarone resulted in the decrease significantly in these three adhesion molecules described above and Ca^2＋ concentration as well as the livability upper and apoptosis lowel：. CONCLUSION ： CD106, CD62P, CE62E, important inflammational factor of Aβ-induced endothelial injury, may be promotion of the inflammatory scade in vascular endothelial. β-asarone may protect ECV30d cell apoptosis by regulate Ca^2＋ and expression of cell surface markers.