科研之友
微信
新浪微博
Facebook
分享链接
摘要
Objective:To test whether tanshinone ⅡA(Tan ⅡA),a highly valued herb derivative to treat vascular diseases in Chinese medicine,could protect endothelial cells from bacterial endotoxin(lipopolysaccharides,LPS)-induced endothelial injury.Methods:Endothelial cell injury was induced by treating human umbilical vein endothelial cells(HUVECs) with 0.2 μg/mL LPS for 24 h.Y27632 and valsartan were used as positive controls.The effects of tanshinone TJ A on the LPS-induced cell viability and apoptosis rate of HUVECs were tested by flow cytometry,cell migration by transwell,adhesion by a 96-well plate pre-coated with vitronectin and cytoskeleton reorganization by immunofluorescence assay.Rho/Rho kinase(ROCK) pathwayassociated gene and protein expression were examined by microarray assay;quantitative real-time polymerase chain reaction and Western blotting were used to confirm the changes observed by microarray.Results:Tan ⅡA improved cell viability,suppressed apoptosis and protected cells from LPS-induced reductions in cell migration and adhesion at a comparable magnitude to that of Y27632 and valsartan.Tan ⅡA,Y27632 and valsartan also normalized LPS-induced actomyosin contraction and vinculin protein aggregation.A microarray assay revealed increased levels of fibronectin,integrin A5(ITG A5),Ras homolog gene family member A(RhoA),myosin light chain phosphatase,phosphatidylinositol-4,5-bisphosphate 3-kinase(PI3K,or PIP2 in Western blotting),focal adhesion kinase,vascular endothelial growth factor and vascular endothelial growth factor receptor 2 in the damaged HUVECs,which were attenuated to different degrees by Tan ⅡA,Y27632 and valsartan.Conclusion:Tan ⅡA exerted a strong protective effect on HUVECs,and the mechanism was caused,at least in part,by a blockade in the Rho/ROCK pathway,presumably through the down-regulation of ITG A5.
- 出版日期2015-5-15
- 单位南京中医药大学
