FOLLOWUS
1. Nanjing University of Chinese Medicine,Nanjing,China
2. Jiangsu Province Hospital of Traditional Chinese Medicine,Nanjing,China
3. Affiliated Hospital of Shandong University of Traditional Chinese Medicine,Jinan,China
纸质出版日期:2014,
网络出版日期:2014-3-4,
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Li, W., Sun, W., Yang, Ch. et al. Tanshinone II a protects against lipopolysaccharides-induced endothelial cell injury via Rho/Rho kinase pathway., Chin. J. Integr. Med. 20, 216–223 (2014). https://doi.org/10.1007/s11655-013-1380-3
Wei Li, Wei Sun, Chuan-hua Yang, et al. Tanshinone II a protects against lipopolysaccharides-induced endothelial cell injury via Rho/Rho kinase pathway[J]. Chinese Journal of Integrative Medicine, 2014,20(3):216-223.
Li, W., Sun, W., Yang, Ch. et al. Tanshinone II a protects against lipopolysaccharides-induced endothelial cell injury via Rho/Rho kinase pathway., Chin. J. Integr. Med. 20, 216–223 (2014). https://doi.org/10.1007/s11655-013-1380-3 DOI:
Wei Li, Wei Sun, Chuan-hua Yang, et al. Tanshinone II a protects against lipopolysaccharides-induced endothelial cell injury via Rho/Rho kinase pathway[J]. Chinese Journal of Integrative Medicine, 2014,20(3):216-223. DOI: 10.1007/s11655-013-1380-3.
To test whether tanshinone II A (Tan II A)
a highly valued herb derivative to treat vascular diseases in Chinese medicine
could protect endothelial cells from bacterial endotoxin (lipopolysaccharides
LPS)-induced endothelial injury. 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 II 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. Tan II A 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 II A
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 II A
Y27632 and valsartan. Conclusion: Tan II A 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.
To test whether tanshinone II A (Tan II A)
a highly valued herb derivative to treat vascular diseases in Chinese medicine
could protect endothelial cells from bacterial endotoxin (lipopolysaccharides
LPS)-induced endothelial injury. 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 II 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. Tan II A 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 II A
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 II A
Y27632 and valsartan. Conclusion: Tan II A 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.
tanshinone II Ahuman umbilical vein endothelial cellsRho/Rho kinase pathway
tanshinone II Ahuman umbilical vein endothelial cellsRho/Rho kinase pathway
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