δ-Tocopherol prevents methylglyoxal-induced apoptosis by reducing ROS generation and inhibiting apoptotic signaling cascades in human umbilical vein endothelial cells

2015 ◽  
Vol 6 (5) ◽  
pp. 1568-1577 ◽  
Author(s):  
Moon ho Do ◽  
Su nam Kim ◽  
Seung-Yong Seo ◽  
Eui-Ju Yeo ◽  
Sun Yeou Kim
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Signaling Cascades ◽  
Ros Generation ◽  
Human Umbilical Vein ◽  
Apoptotic Signaling ◽  
Apoptotic Activity ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

δ-Tocopherol protects HUVECs against apoptotic activity induced by methylglyoxal.

scholarly journals Polydatin Prevents Methylglyoxal-Induced Apoptosis through Reducing Oxidative Stress and Improving Mitochondrial Function in Human Umbilical Vein Endothelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Ningbo Pang ◽  
Tangting Chen ◽  
Xin Deng ◽  
Ni Chen ◽  
Rong Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Mitochondrial Function ◽  
Cell Apoptosis ◽  
Umbilical Vein ◽  
Ros Generation ◽  
Mitochondrial Morphology ◽  
Human Umbilical Vein ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

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.

scholarly journals Upregulation of Periostin Prevents High Glucose-Induced Mitochondrial Apoptosis in Human Umbilical Vein Endothelial Cells via Activation of Nrf2/HO-1 Signaling

2016 ◽  
Vol 39 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Zhi-ying Zhong ◽  
Yu Tang
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Umbilical Vein ◽  
Vascular Complications ◽  
Ros Generation ◽  
Mitochondrial Apoptosis ◽  
Human Umbilical Vein ◽  
Diabetic Vascular Complications ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

Background/Aims: High glucose-induced oxidative damage to endothelial cells plays a central role in the pathogenesis of diabetic vascular complications. This study was undertaken to explore the role of periostin in high glucose-induced endothelial cell apoptosis and associated molecular mechanisms. Methods: Human umbilical vein endothelial cells (HUVECs) were exposed to high glucose (33.3 mmol/L) and examined for the expression of periostin. The effects of periostin upregulation on high glucose-induced apoptosis, mitochondrial dysfunction, and reactive oxygen species (ROS) production were determined. The activation of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) by periostin was checked. HO-1 knockdown experiments were done to confirm its role in the action of periostin in high glucose-exposed HUVECs. Results: High glucose significantly upregulated the expression of periostin in HUVECs. Enforced expression of periostin attenuated high glucose-induced apoptosis in HUVECs, as determined by TUNEL staining and caspase-3 activity assay. Periostin overexpression prevented loss of Δψm, release of mitochondrial cytochrome c, and dysregulation of Bcl-2 and Bax in high glucose-exposed HUVECs. Periostin upregulation suppressed high glucose-induced ROS generation and activated the Nrf2/HO-1 signaling. HO-1 silencing restored high glucose-induced ROS generation and apoptotic response in periostin-overexpressing HUVECs. Conclusion: Periostin mitigates high glucose-induced mitochondrial apoptosis in endothelial cells, via activation of Nrf2/HO-1 signaling and reduction of ROS formation. Further studies are warranted to explore the therapeutic potential of periostin in diabetic vascular complications.

scholarly journals Protective effects of hyperoside against H2O2-induced apoptosis in human umbilical vein endothelial cells

2016 ◽  
Vol 14 (1) ◽  
pp. 399-405 ◽  
Author(s):  
XU-LIANG HAO ◽  
YA KANG ◽  
JIAN-KUAN LI ◽  
QING-SHAN LI ◽  
EN-LI LIU ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Protective Effects ◽  
Human Umbilical Vein ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells
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