Tanshinone II a protects against lipopolysaccharides-induced endothelial cell injury via Rho/Rho kinase pathway

Wei Li; Wei Sun; Chuan-hua Yang; Hong-zhen Hu; Yue-hua Jiang

doi:10.1007/s11655-013-1380-3

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Tanshinone II a protects against lipopolysaccharides-induced endothelial cell injury via Rho/Rho kinase pathway

Updated：2021-08-27

- Tanshinone II a protects against lipopolysaccharides-induced endothelial cell injury via Rho/Rho kinase pathway
- Chinese Journal of Integrative Medicine Vol. 20, Issue 3, Pages: 216-223(2014)
- Affiliations：
  
  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
- Author bio：
- Funds：
  
  Supported by Science and Technology Development Plan of Shandong Province (No. 2012G0021837)
- DOI：10.1007/s11655-013-1380-3
  CLC：
- Published：2014，
  
  Published Online：4 March 2014，
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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 20(3):216-223(2014)
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 20(3):216-223(2014) DOI： 10.1007/s11655-013-1380-3.

摘要

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.

Abstract

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

cell migration by transwell

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.

关键词

tanshinone II Ahuman umbilical vein endothelial cellsRho/Rho kinase pathway

Keywords

tanshinone II Ahuman umbilical vein endothelial cellsRho/Rho kinase pathway

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Integrative Hospital, College of Chinese Medicine, Southern Medical University

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Department of Emergency, First Affiliated Hospital to Jiangxi Medical College

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