Dimethyl sulfoxide induces heme oxygenase-1 expression via JNKs and Nrf2 pathways in human umbilical vein endothelial cells

2011 ◽  
Vol 355 (1-2) ◽  
pp. 109-115 ◽  
Author(s):  
Chao Liang ◽  
Zhanggang Xue ◽  
Jing Cang ◽  
Hao Wang ◽  
Ping Li
Keyword(s):  
Endothelial Cells ◽  
Dimethyl Sulfoxide ◽  
Heme Oxygenase ◽  
Umbilical Vein ◽  
Heme Oxygenase 1 ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Hemin-induced Erk1/2 activation and heme oxygenase-1 expression in human umbilical vein endothelial cells

2007 ◽  
Vol 41 (9) ◽  
pp. 990-996 ◽  
Author(s):  
Nan Chen ◽  
Wei Shao ◽  
Pingping Lv ◽  
Shuluo Zhang ◽  
Yingying Chen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Heme Oxygenase ◽  
Umbilical Vein ◽  
Heme Oxygenase 1 ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Heme oxygenase-1 is an important modulator in limiting glucose-induced apoptosis in human umbilical vein endothelial cells

Life Sciences ◽  
2008 ◽  
Vol 82 (7-8) ◽  
pp. 383-392 ◽  
Author(s):  
Elisabetta Iori ◽  
Elisa Pagnin ◽  
Alessandra Gallo ◽  
Lorenzo Calò ◽  
Ellen Murphy ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Heme Oxygenase ◽  
Umbilical Vein ◽  
Heme Oxygenase 1 ◽  
Human Umbilical Vein ◽  
Induced Apoptosis ◽  
Umbilical Vein Endothelial Cells

scholarly journals Cytoprotective Role of Edible Seahorse (Hippocampus abdominalis)-Derived Peptides in H2O2-Induced Oxidative Stress in Human Umbilical Vein Endothelial Cells

Marine Drugs ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 86
Author(s):  
Yunok Oh ◽  
Chang-Bum Ahn ◽  
Jae-Young Je
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Combination Treatment ◽  
Umbilical Vein ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Nuclear Staining ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Oxidative stress-induced endothelial dysfunction is strongly linked to the pathogenesis of cardiovascular diseases. A previous study revealed that seahorse hydrolysates ameliorated oxidative stress-mediated human umbilical vein endothelial cells (HUVECs) injury. However, the responsible compounds have not yet been identified. This study aimed to identify cytoprotective peptides and to investigate the molecular mechanism underlying the cytoprotective role in H2O2-induced HUVECs injury. After purification by gel filtration and HPLC, two peptides were sequenced by liquid chromatography-tandem mass spectrometry as HGSH (436.43 Da) and KGPSW (573.65 Da). The synthesized peptides and their combination (1:1 ratio) showed significant HUVECs protection effect at 100 μg/mL against H2O2-induced oxidative damage via significantly reducing intracellular reactive oxygen species (ROS). Two peptides and their combination treatment resulted in the increased heme oxygenase-1 (HO-1), a phase II detoxifying enzyme, through the activation of nuclear transcription factor-erythroid 2-related factor (Nrf2). Additionally, cell cycle and nuclear staining analysis revealed that two peptides and their combination significantly protected H2O2-induced cell death through antiapoptotic action. Two peptides and their combination treatment led to inhibit the expression of proapoptotic Bax, the release of cytochrome C into the cytosol, the activation of caspase 3 by H2O2 treatment in HUVECs, whereas antiapoptotic Bcl-2 expression was increased with concomitant downregulation of Bax/Bcl-2 ratio. Taken together, these results suggest that seahorse-derived peptides may be a promising agent for oxidative stress-related cardiovascular diseases.

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