Protective effects of Tinospora crispa extracts on H2O2-induced oxidative stress and TNF-α-induced inflammation on human umbilical vein endothelial cells (HUVECs)

2012 ◽  
Vol 6 (15) ◽  
Author(s):  
Ihsan Safwan Kamarazaman
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Protective Effects ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells

Protective effects of peoniflorin against hydrogen peroxide-induced oxidative stress in human umbilical vein endothelial cells

2011 ◽  
Vol 89 (6) ◽  
pp. 445-453 ◽  
Author(s):  
Tao Chen ◽  
Zai-pei Guo ◽  
Xiao-yan Jiao ◽  
Yu-hong Zhang ◽  
Jing-yi Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Endothelial Cells ◽  
Oxidative Damage ◽  
Umbilical Vein ◽  
Flow Cytometric Analysis ◽  
Vascular Diseases ◽  
Protective Effects ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Peoniflorin (PF), extracted from the root of Paeonia lactiflora Pall., has been reported to have anti-inflammation and antioxidant effects in several animal models. Herein, we investigated the protective effects of PF against hydrogen peroxide (H2O2)-induced oxidative damage in human umbilical vein endothelial cells (HUVECs). HUVECs were treated by H2O2 (240 µmol/L) with or without PF. PF significantly increased the percent cell viability of HUVECs injured by H2O2 using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. By flow cytometric analysis, PF markedly attenuated H2O2-induced apoptosis and intracellular reactive oxygen species production. In addition, PF also displayed a dose-dependent reduction of lactate dehydrogenase leakage, malondialdehyde formation, and caspase-3 proteolytic activities in H2O2-treated cells, which was accompanied with a restoration of the activities of endogenous antioxidants, including total superoxide dismutase and glutathione peroxidase. Finally, Western blot data revealed that H2O2 upregulated phosphorylation of extracellular signal-regulated kinase 1/2 in HUVECs, which was almost completely reversed by PF. Taken together, our data provide the first evidence that PF has a protective ability against oxidative damage in HUVECs. PF may be a candidate medicine for the treatment of vascular diseases associated with oxidative stress.

scholarly journals Protective Effects of Crocetin on Arsenic Trioxide-induced Oxidative Stress in Human Umbilical Vein Endothelial Cells

In Vivo ◽  
2021 ◽  
Vol 35 (6) ◽  
pp. 3157-3163
Author(s):  
CHUNG-LIN TSAI ◽  
CHIA-WEN TSAI ◽  
WEN-SHIN CHANG ◽  
JIUNN-CHERNG LIN ◽  
LIANG-CHUN SHIH ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Arsenic Trioxide ◽  
Umbilical Vein ◽  
Protective Effects ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

scholarly journals Brazilian Green Propolis Inhibits Ox-LDL-Stimulated Oxidative Stress in Human Umbilical Vein Endothelial Cells Partly through PI3K/Akt/mTOR-Mediated Nrf2/HO-1 Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Wenwen Yuan ◽  
Huasong Chang ◽  
Xinying Liu ◽  
Shiqiang Wang ◽  
Hui Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Nuclear Translocation ◽  
Umbilical Vein ◽  
Heme Oxygenase 1 ◽  
Protective Effects ◽  
Gene Expressions ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Brazilian Green Propolis

Propolis has been widely used as a dietary supplement for its health benefits, including cardiovascular protective effects. The aim of this study was to investigate the cytoprotective effects of Brazilian green propolis (BP) against oxidized low-density lipoprotein (Ox-LDL) induced human umbilical vein endothelial cells (HUVECs) damage. Our results suggested that treatment with BP rescued Ox-LDL-stimulated HUVECs cell viability losses, which might be associated with its inhibitive effects on the cell apoptosis and autophagy. We also noticed that BP restored Ox-LDL-stimulated HUVECs oxidative stress, by induced antioxidant gene expressions, including Heme oxygenase-1 and its upstream mediator, Nrf2, which were mediated by the activation of the phosphorylation of PI3K/Akt/mTOR. Pretreatment with wortmannin, PI3K/AKT inhibitor, abolished BP induced Nrf2 nuclear translocation and HO-1 level. Our results demonstrated that BP protected HUVECs against oxidative damage partly via PI3K/Akt/mTOR-mediated Nrf/HO-1 pathway, which might be applied into preventing Ox-LDL mediated cardiovascular diseases.

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