Protective effects of phenolic acid extract from ginseng on vascular endothelial cell injury induced by palmitate via activation of PI3K/Akt/eNOS pathway

2020 ◽  
Vol 85 (3) ◽  
pp. 576-581
Author(s):  
Xuenan Chen ◽  
Fan Yao ◽  
Jia Song ◽  
Baoyu Fu ◽  
Guang Sun ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Phenolic Acid ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Acid Extract ◽  
Endothelial Cell Injury

scholarly journals Microparticulate Caspase 1 Regulates Gasdermin D and Pulmonary Vascular Endothelial Cell Injury

2018 ◽  
Vol 59 (1) ◽  
pp. 56-64 ◽  
Author(s):  
Srabani Mitra ◽  
Matthew Exline ◽  
Fabien Habyarimana ◽  
Mikhail A. Gavrilin ◽  
Paul J. Baker ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury ◽  
Caspase 1

scholarly journals Blocking the REDD1/TXNIP axis ameliorates LPS-induced vascular endothelial cell injury through repressing oxidative stress and apoptosis

2019 ◽  
Vol 316 (1) ◽  
pp. C104-C110 ◽  
Author(s):  
Xuhui Hou ◽  
Songbai Yang ◽  
Jian Yin
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Reactive Oxygen Species Generation ◽  
Vascular Endothelial ◽  
Interacting Protein ◽  
Endothelial Cell Injury ◽  
Lactate Dehydrogenase Release

The aim of the present study was to investigate the potential role of regulated in development and DNA damage response 1 (REDD1) in LPS-induced vascular endothelial injury by using human umbilical vein endothelial cells (HUVECs). We observed that REDD1 expression was apparently elevated in HUVECs after exposure to LPS. Additionally, elimination of REDD1 strikingly attenuated the secretion of the proinflammatory cytokines TNF-α, IL-6, IL-1β, and monocyte chemotactic protein-1 and the endothelial cell adhesion markers ICAM-1 and VCAM-1 that was induced by LPS stimulation. Subsequently, knockdown of REDD1 augmented cell viability but ameliorated lactate dehydrogenase release in HUVECs stimulated with LPS. Meanwhile, depletion of REDD1 effectively restricted LPS-induced HUVEC apoptosis, as exemplified by reduced DNA fragmentation, and it also elevated antiapoptotic Bcl-2 protein, concomitant with reduced levels of proapoptotic proteins Bax and cleaved caspase-3. Furthermore, repression of REDD1 remarkably alleviated LPS-triggered intracellular reactive oxygen species generation accompanied by decreased malondialdehyde content and increased the activity of the endogenous antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase. Most important, depletion of REDD1 protected HUVECs against inflammation-mediated apoptosis and oxidative damage partly through thioredoxin-interacting protein (TXNIP). Collectively, these findings indicate that blocking the REDD1/TXNIP axis repressed the inflammation-mediated vascular injury process, which may be closely related to oxidative stress and apoptosis in HUVECs, implying that the REDD1/TXNIP axis may be a new target for preventing the endothelial cell injury process.

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