Esterification Enhanced Intestinal Absorption of Ginsenoside Rh2 in Caco-2 Cells without Impacts on Its Protective Effects against H2O2-Induced Cell Injury in Human Umbilical Vein Endothelial Cells (HUVECs)

2014 ◽  
Vol 62 (9) ◽  
pp. 2096-2103 ◽  
Author(s):  
Bing Zhang ◽  
Hui Ye ◽  
Xue-Mei Zhu ◽  
Jiang-Ning Hu ◽  
Hong-Yan Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Intestinal Absorption ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Protective Effects ◽  
Ginsenoside Rh2 ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

scholarly journals Baicalin Protects against Thrombin-Induced Cell Injury in Human Umbilical Vein Endothelial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Anna Zhang ◽  
Yunfeng Hou ◽  
Chao Sun ◽  
Ying Pu ◽  
Yu Sun ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Pivotal Role ◽  
Flavonoid Compound ◽  
Erk Pathway ◽  
Protective Effects ◽  
Human Umbilical Vein ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

Thrombin plays a pivotal role in the pathogenesis of atherosclerosis. Baicalin, an active flavonoid compound, was shown to attenuate the development of atherosclerosis, but the mechanism remains elusive. In the present study, the role and mechanism of baicalin in thrombin-induced cell injury was investigated in human umbilical vein endothelial cells (HUVECs). Our results showed that baicalin significantly reduced thrombin-induced apoptosis of HUVECs. Additional experiments showed that baicalin inhibited thrombin-induced NF-κB activation and PAR-1 expression. In addition, baicalin decreased thrombin-induced PAR-1 expression by inhibiting ERK pathway. These results indicated that baicalin has protective effects on thrombin-induced cell injury in HUVECs possibly through inhibition of PAR-1 expression and its downstream NF-κB activation, which was mediated by ERK1/2 activation.

scholarly journals CTRP3 Protects against High Glucose-Induced Cell Injury in Human Umbilical Vein Endothelial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Fang Wang ◽  
Linlin Zhao ◽  
Yingguang Shan ◽  
Ran Li ◽  
Guijun Qin
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Cell Loss ◽  
Inflammatory Factors ◽  
Therapeutic Drug ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Aims. Inflammation was closely associated with diabetes-related endothelial dysfunction. C1q/tumor necrosis factor-related protein 3 (CTRP3) is a member of the CTRP family and can provide cardioprotection in many cardiovascular diseases via suppressing the production of inflammatory factors. However, the role of CTRP3 in high glucose- (HG-) related endothelial dysfunction remains unclear. This study evaluates the effects of CTRP3 on HG-induced cell inflammation and apoptosis. Materials and Methods. To prevent high glucose-induced cell injury, human umbilical vein endothelial cells (HUVECs) were pretreated with recombinant CTRP3 for 1 hour followed by normal glucose (5.5 mmol/l) or high glucose (33 mmol/l) treatment. After that, cell apoptosis and inflammatory factors were determined. Results. Our results demonstrated that CTRP3 mRNA and protein expression were significantly decreased after HG exposure in HUVECs. Recombinant human CTRP3 inhibited HG-induced accumulation of inflammatory factors and cell loss in HUVECs. CTRP3 treatment also increased the phosphorylation levels of protein kinase B (AKT/PKB) and the mammalian target of rapamycin (mTOR) in HUVECs. CTRP3 lost its inhibitory effects on HG-induced cell inflammation and apoptosis after AKT inhibition. Knockdown of endogenous CTRP3 in HUVECs resulted in increased inflammation and decreased cell viability in vitro. Conclusions. Taken together, these findings indicated that CTRP3 treatment blocked the accumulation of inflammatory factors and cell loss in HUVECs after HG exposure through the activation of AKT-mTOR signaling pathway. Thus, CTRP3 may be a potential therapeutic drug for the prevention of diabetes-related endothelial dysfunction.

scholarly journals Curcumin Protects Human Umbilical Vein Endothelial Cells against H2O2-Induced Cell Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Jipeng Ouyang ◽  
Rong Li ◽  
Haiqin Shi ◽  
Jianping Zhong
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cell Death ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Therapeutic Drug ◽  
Human Umbilical Vein ◽  
Antioxidative Enzyme Activities ◽  
Apoptosis Related Protein ◽  
Umbilical Vein Endothelial Cells

Migraine is a prevalent neurological disorder which causes a huge economic burden on society. It is thought to be a neurovascular disease with oxidative stress might be involved. Curcumin, one of the major ingredients of turmeric, has potent antioxidative and anti-inflammatory properties, but whether it could be used as a potential treatment for migraine remains to be explored. In the present study, human umbilical vein endothelial cells (HUVECs) were pretreated with various concentrations of curcumin (0 μM, 10 μM, 20 μM, 30 μM, 40 μM, and 50 μM) for 12 h, thereby exposed to H2O2 (100 μM) for another 12 h. The viability of HUVECs was tested by the CCK-8 assay, and the activities of antioxidant enzymes including superoxide dismutase (SOD) and glutathione (GSH) were also examined. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were assayed to determine H2O2-induced oxidative stress. In addition, several cell death-related genes (p53, p21, Bax, and Bcl-2) were detected by PCR, and an apoptosis-related protein (caspase3) was evaluated by western blotting. Our results showed that curcumin improved the H2O2-induced decrease of cell viability and antioxidative enzyme activities and decreased the level of oxidative stress. As a conclusion, curcumin could mitigate H2O2-induced oxidative stress and cell death in HUVECs and may be a potential therapeutic drug for migraine.

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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