scholarly journals GW25-e5306 Hydroxysafflor yellow A protects against the particulate matter (PM2.5) -induced cell injury by modulating intracellular redox via Nrf2/Keap1 pathway in Human umbilical vein endothelial cells

2014 ◽  
Vol 64 (16) ◽  
pp. C32
Author(s):  
Li Caiping ◽  
Ji-yuan Lv
Keyword(s):  
Endothelial Cells ◽  
Particulate Matter ◽  
Cell Injury ◽  
Umbilical Vein ◽  
Hydroxysafflor Yellow A ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Intracellular Redox

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 Hydroxysafflor Yellow A Attenuates Hydrogen Peroxide-Induced Oxidative Damage on Human Umbilical Vein Endothelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Yuefeng Xie ◽  
Yan Guo ◽  
ShiDong Cao ◽  
Miaomiao Xue ◽  
ZhaoYue Fan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Chinese Medicine ◽  
Cardiovascular Diseases ◽  
Traditional Chinese Medicine ◽  
Oxidative Damage ◽  
Umbilical Vein ◽  
Hydroxysafflor Yellow A ◽  
Sod Activity ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Oxidative stress of endothelial cells is thought to be a principal cause that induces many cardiovascular diseases. Hydroxysafflor yellow A (HSYA) is a major active component in traditional Chinese medicine safflower and has been used to cure ischemic cardiovascular diseases in China for many years. This study aims to investigate whether HSYA has a repairing effect on oxidative damage of human umbilical vein endothelial cells (HUVECs) induced by H2O2 and to provide a theoretical basis for the clinical treatment of cardiovascular diseases related to traditional Chinese medicine. Based on the establishment of an H2O2-induced HUVEC oxidative injury model, the cell viability and proliferation rate were measured by the MTT assay and EdU staining. The intracellular GSH/GSSG ratio and SOD activity were determined by kits. The ROS level was detected by flow cytometry. And the BAX, Bcl-2, PTEN, and AKT expressions were evaluated with western blotting methods. The results showed that HSYA treatment significantly attenuated the H2O2-induced HUVEC cell damage, increased the intracellular GSH/GSSG ratio and unit SOD activity also, and decreased the intracellular ROS levels. Furthermore, HSYA increased the expressions of AKT and Bcl-2 proteins and inhibited the expressions of BAX and PTEN proteins. These suggest that HSYA exerts repair effects on H2O2-induced oxidative damage in HUVECs, and the mechanisms may be related to the influence of BAX/Bcl-2 expression and AKT/PTEN signal pathway expression.

Sign in / Sign up

Export Citation Format

Share Document