Paeoniflorin attenuates oxidized low‐density lipoprotein‐induced apoptosis and adhesion molecule expression by autophagy enhancement in human umbilical vein endothelial cells

2018 ◽  
Vol 120 (6) ◽  
pp. 9291-9299 ◽  
Author(s):  
Yi Wang ◽  
Jianbo Che ◽  
Hui Zhao ◽  
Jianyu Tang ◽  
Gongning Shi
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Umbilical Vein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Adhesion Molecule Expression ◽  
Oxidized Low Density Lipoprotein ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

scholarly journals Tongxinluo Regulates Expression of Tight Junction Proteins and Alleviates Endothelial Cell Monolayer Hyperpermeability via ERK-1/2 Signaling Pathway in Oxidized Low-Density Lipoprotein-Induced Human Umbilical Vein Endothelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Chengcheng Chang ◽  
Hongli Liu ◽  
Cong Wei ◽  
Liping Chang ◽  
Junqing Liang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tight Junction ◽  
Umbilical Vein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Paracellular Permeability ◽  
Low Density ◽  
Vascular Endothelial ◽  
Oxidized Low Density Lipoprotein ◽  
Umbilical Vein Endothelial Cells

Vascular hyperpermeability resulting from distortion of endothelial junctions is associated with a number of cardiovascular diseases. Endothelial tight junction regulates the paracellular permeability of macromolecules, a function ofHuman Umbilical Vein Endothelial Cells(HUVEC) monolayers that can be regulated byoxidized Low-density Lipoprotein(ox-LDL). However, the understanding of drug regulation of vascular hyperpermeability is so far limited. This study thus aimed to investigate the role ofTongxinluo(TXL) in the maintenance of the vascular endothelial paracellular permeability. Here, changes in permeability were determined by measuring the paracellular flux of FITC-dextran 40000 (FD40), while protein expression and intercellular distribution were examined by western blot and immunofluorescence assay, respectively. We found that TXL alleviated the ox-LDL-induced increase in flux of FD40 and then reduced the hyperpermeability. Moreover, ox-LDL-induced disruptions of ZO-1, occludin, and claudin1 were also restored. This is via the activation of ERK1/2 in the vascular endothelial cells. Our results provide insights into the molecular mechanism by which TXL alleviates ox-LDL-induced hyperpermeability and provide the basis for further investigations of TXL as regulators of vascular barrier function.

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