Carbofuran cytotoxicity, DNA damage, oxidative stress, and cell death in human umbilical vein endothelial cells: Evidence of vascular toxicity

2021 ◽  
Author(s):  
Quaiser Saquib ◽  
Maqsood A. Siddiqui ◽  
Sabiha M. Ansari ◽  
Hend A. Alwathnani ◽  
Abdulaziz A. Al‐Khedhairy
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Endothelial Cells ◽  
Cell Death ◽  
Umbilical Vein ◽  
Vascular Toxicity ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

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 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.

Lipid mediators of autophagy in stress-induced premature senescence of endothelial cells

2008 ◽  
Vol 294 (3) ◽  
pp. H1119-H1129 ◽  
Author(s):  
Susann Patschan ◽  
Jun Chen ◽  
Alla Polotskaia ◽  
Natalja Mendelev ◽  
Jennifer Cheng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Umbilical Vein ◽  
Acid Sphingomyelinase ◽  
Premature Senescence ◽  
Human Umbilical Vein ◽  
Glycation End Products ◽  
Umbilical Vein Endothelial Cells ◽  
Stress Induced Premature Senescence

Our group (Patschan S, Chen J, Gealekman O, Krupincza K, Wang M, Shu L, Shayman JA, Goligorsky MS; Am J Physiol Renal Physiol 294: F100–F109, 2008) previously observed an accumulation of gangliosides coincident with development of cell senescence and demonstrated lysosomal permeabilization in human umbilical vein endothelial cells exposed to glycated collagen I (GC). Therefore, we investigated whether the lysosome-dependent, caspase-independent or type 2-programmed cell death (autophagy) is involved in development of premature senescence of endothelial cells. The cleaved microtubule-associated protein 1 light-chain 3 (LC3), a marker of autophagosome formation, was overexpressed within 24 h of GC treatment; however, by 4–5 days, it was nearly undetectable. Early induction of autophagosomes was associated with their fusion with lysosomes, a phenomenon that later became subverted. Autophagic cell death can be triggered by the products of damaged plasma membrane, sphingolipids, and ceramide. We observed a clustering of membrane rafts shortly after exposure to GC; later, after 24 h, we observed an internalization, accompanied by an increased acid sphingomyelinase activity and accumulation of ceramide. Pharmacological inhibition of autophagy prevented development of premature senescence but did lead to the enhanced rate of apoptosis in human umbilical vein endothelial cells exposed to GC. Pharmacological induction of autophagy resulted in reciprocal changes. These observations appear to represent a mechanistic molecular cascade whereby advanced glycation end products like GC induce sphingomyelinase activity, accumulation of ceramide, clustering, and later internalization of lipid rafts.

Coenzyme Q10 prevents high glucose-induced oxidative stress in human umbilical vein endothelial cells

2007 ◽  
Vol 566 (1-3) ◽  
pp. 1-10 ◽  
Author(s):  
Hiroshi Tsuneki ◽  
Naoto Sekizaki ◽  
Takashi Suzuki ◽  
Shinjiro Kobayashi ◽  
Tsutomu Wada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Coenzyme Q10 ◽  
High Glucose ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells
Sign in / Sign up

Export Citation Format

Share Document