scholarly journals EGCG Regulates Cell Apoptosis of Human Umbilical Vein Endothelial Cells Grown on 316L Stainless Steel for Stent Implantation

2021 ◽  
Vol Volume 15 ◽  
pp. 493-499
Author(s):  
Jinpeng Wang ◽  
Yue Wang ◽  
Yuyi Zhao ◽  
Jinbin Zhao ◽  
Beilin Zhang ◽  
...  
2015 ◽  
Vol 3 (44) ◽  
pp. 8717-8728 ◽  
Author(s):  
Xin Li ◽  
Shuheng Yuan ◽  
Si Chen ◽  
Rifang Luo ◽  
Kaiqin Xiong ◽  
...  

An angiopoietin-1 functionalized surface was establishedviapolydopamine coating and regulated HUVECs survival, proliferation and function.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Ningbo Pang ◽  
Tangting Chen ◽  
Xin Deng ◽  
Ni Chen ◽  
Rong Li ◽  
...  

Methylglyoxal (MGO), an active metabolite of glucose, has been reported to induce vascular cell apoptosis in diabetic complication. Polydatin (PD), a small natural compound from Polygonum cuspidatum, has a number of biological functions, such as antioxidative, anti-inflammatory, and nephroprotective properties. However, the protective effects of PD on MGO-induced apoptosis in endothelial cells remain to be elucidated. In this study, human umbilical vein endothelial cells (HUVECs) were used to explore the effects of PD on MGO-induced cell apoptosis and the possible mechanism involved. HUVECs were pretreated with PD for 2 h, followed by stimulation with MGO. Then cell apoptosis, reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP) impairment, mitochondrial morphology alterations, and Akt phosphorylation were assessed. The results demonstrated that PD significantly prevented MGO-induced HUVEC apoptosis. PD pretreatment also significantly inhibited MGO-induced ROS production, MMP impairment, mitochondrial morphology changes, and Akt dephosphorylation. These results and the experiments involving N-acetyl cysteine (antioxidant), Cyclosporin A (mitochondrial protector), and LY294002 (Akt inhibitor) suggest that PD prevents MGO-induced HUVEC apoptosis, at least in part, through inhibiting oxidative stress, maintaining mitochondrial function, and activating Akt pathway. All of these data indicate the potential application of PD for the treatment of diabetic vascular complication.


2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Lei Li ◽  
Jiafeng Lin ◽  
Maoping Chu ◽  
Kangting Ji ◽  
Lianpin Wu

A20, a negative regulator of nuclear factor κB signaling, has been shown to attenuate atherosclerotic events. Transforming growth factor beta-activated kinase 1 (TAK1) plays a critical role in TNFα-induced atherosclerosis via endothelial nitric oxide (NO) synthase (eNOS) uncoupling and NO reduction. Aims: In the study, we investigated the hypothesis that A20 protected endothelial cells induced by TNFα through modulating eNOS activity and TAK1 signalling. Human umbilical vein endothelial cells (HUVECs) were stimulated by TNFα. The impact of A20 on cell apoptosis, eNOS expression and NO production and related TAK1 pathway were detected. Both eNOS and NO production were remarkably reduced, TAK1and p38 MAPK phosphorylation, HUVECs apoptosis increased after TNFα stimulation for 2 hrs, all of which were effectively attenuated by A20 over-expression. Inhibition of A20 significantly activated TAK1, p38 MAPK phosphorylation, and cell apoptosis, but eNOS expression, NO production decreased. Furthermore, p38 MAPK expression was suppressed by A20 over-expression, but re-enhanced by inhibiting A20 or activation of TAK1. Furtherly, TNFα-induced suppression of eNOS and NO production were largely prevented by silencing p38 MAPK. Collectively, our results suggested that A20-mediated TAK1 inactivation suppresses p38 MAPK and regulated MAPK/eNOS pathway, which contributes to endothelial cell survival and function preservation.


2017 ◽  
Vol 444 (1-2) ◽  
pp. 77-86 ◽  
Author(s):  
Shanshan Cui ◽  
Wen Li ◽  
Pengyan Wang ◽  
Xin Lv ◽  
Yuxia Gao ◽  
...  

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