Titanate nanotubes at non-cytotoxic concentrations affect NO signaling pathway in human umbilical vein endothelial cells

2020 ◽  
Vol 62 ◽  
pp. 104689 ◽  
Author(s):  
Shuang Li ◽  
Hongji Liu ◽  
Zhengzheng Zhou ◽  
Yi Cao
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Titanate Nanotubes ◽  
Human Umbilical Vein ◽  
No Signaling ◽  
Umbilical Vein Endothelial Cells

scholarly journals Sodium tanshinone IIA sulfonate prevents lipopolysaccharide-induced inflammation via suppressing nuclear factor-κB signaling pathway in human umbilical vein endothelial cells

2018 ◽  
Vol 96 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Jun Cheng ◽  
Tangting Chen ◽  
Pengyun Li ◽  
Jing Wen ◽  
Ningbo Pang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Nuclear Factor Κb ◽  
Tanshinone Iia ◽  
Nuclear Factor ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Sodium Tanshinone Iia Sulfonate ◽  
Umbilical Vein Endothelial Cells

Sodium tanshinone IIA sulfonate (STS), a water-soluble derivative of tanshinone IIA, has been demonstrated to have potent anti-inflammatory properties. However, the protective effects of STS on lipopolysaccharide (LPS)-induced inflammation in endothelial cells remain to be elucidated. In the present study, human umbilical vein endothelial cells (HUVECs) were used to explore the effects of STS on LPS-induced inflammation and the molecular mechanism involved. HUVECs were pretreated with STS for 2 h, followed by stimulation with LPS. Then expression and secretion of tumor necrosis factor (TNF)-α and interleukin (IL)-1β, and the activation of nuclear factor-κB (NF-κB) were assessed. The results demonstrated that STS significantly decreased LPS-induced TNF-α and IL-1β protein expression in HUVECs. Similarly, the increased levels of TNF-α and IL-1β in cell supernatants stimulated by LPS were also significantly inhibited by STS. Furthermore, STS inhibited LPS-induced NF-κB p65 phosphorylation and nuclear translocation. All the results suggest that STS prevents LPS-induced inflammation through suppressing NF-κB signaling pathway in endothelial cells, indicating the potential utility of STS for the treatment of inflammatory diseases.

scholarly journals Paeoniflorin Suppresses TBHP-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells via the Nrf2/HO-1 Signaling Pathway and Improves Skin Flap Survival

2021 ◽  
Vol 12 ◽  
Author(s):  
Jingtao Jiang ◽  
Chengji Dong ◽  
Liang Zhai ◽  
Junsheng Lou ◽  
Jie Jin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Skin Flap ◽  
Random Pattern ◽  
Heme Oxygenase 1 ◽  
Ros Production ◽  
Flap Survival ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Random-pattern skin flap is a vital technique frequently applied in reconstruction surgeries for its convenience and effectiveness in solving skin defects. However, ischemic necrosis, especially in the distal areas of the flap, still needs extra attention after surgery. Earlier evidence has suggested that paeoniflorin (PF) could stimulate angiogenesis and suppress ischemic cardiovascular disease. However, few studies have focused on the role of PF in flap survival. In this study, we have demonstrated that the human umbilical vein endothelial cells (HUVECs) treated with PF can alleviate tert-butyl hydroperoxide (TBHP)-stimulated cellular dysfunction and apoptosis. To better evaluate, HUVECs’ physiology, cell tube formation, migration, and adhesion were assessed. Mechanistically, PF protects HUVECs against apoptosis via stimulating the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway. PF also downregulates mitochondrial ROS production to reduce excessive intracellular ROS production induced by TBHP and restore TBHP-induced mitochondrial depolarization. As a result, silencing Nrf2 partially abolishes the protective effect of PF exposure on HUVECs. In in vivo experiments, the oral administration of PF was shown to have enhanced the vascularization of regenerated tissues and promote flap survival. However, the PF-mediated protection was partially lost after co-treatment with ML385, a selective Nrf2 inhibitor, suggesting that PF is a crucial modulator regulating the Nrf2/HO-1 signaling pathway. In summary, our data have provided a new insight into PF as a potential therapy for enhancing random-pattern flap viability.

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