scholarly journals Combination of Astragalus membranaceous and Angelica sinensis Ameliorates Vascular Endothelial Cell Dysfunction by Inhibiting Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Yonghui Yin ◽  
Hui Li ◽  
Yumin Chen ◽  
Ranran Zhu ◽  
Li Li ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Cell Migration ◽  
High Glucose ◽  
Migration And Invasion ◽  
Angelica Sinensis ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Cell Migration And Invasion ◽  
Diabetic Macroangiopathy

Vascular endothelial dysfunction is an essential and early sign of diabetic macroangiopathy, a primary complication of diabetes mellitus. Astragalus membranaceous-Angelica sinensis is a classic medical combination applied in China to treat diabetes mellitus. The aim of this study was to investigate the effect of the granule form of the extract produced from the dried root of Astragalus membranaceous (AM) combination with the granule form of the extract produced from the dried Angelica sinensis (AS) on diabetic macroangiopathy and its underlying mechanism. Herein, rats were treated by AM-AS at a ratio of 3 : 2 via intragastric administration. High glucose-induced human umbilical vein vascular endothelial cells (HUVECs) were then treated with drug-containing serum collected from the rats. In high glucose-treated HUVECs, AM-AS combination increased cell viability (P<0.05), decreased the percentage of apoptotic cells (P<0.05) and the expression of the proapoptosis protein caspase 3 (P<0.05), reduced the proportion of cells in the G0/G1 phase (P<0.05), decreased reactive oxygen species level (P<0.05), enhanced cell migration and invasion (P<0.05), and reduced the level of 8-iso-prostaglandin F2alpha. These results indicate that AM-AS combination at the ratio of 3 : 2 ameliorated HUVEC dysfunction by regulating apoptosis, cell migration, and invasion, which might be mediated by their regulatory effect on reactive oxygen species production. The current study provides a theoretical basis for the treatment of diabetic macroangiopathy using AM-AS.

scholarly journals Regulation of Lung Cancer Cell Migration and Invasion by Reactive Oxygen Species and Caveolin-1

2010 ◽  
Vol 285 (50) ◽  
pp. 38832-38840 ◽  
Author(s):  
Sudjit Luanpitpong ◽  
Siera Jo Talbott ◽  
Yon Rojanasakul ◽  
Ubonthip Nimmannit ◽  
Varisa Pongrakhananon ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Cell Migration ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Oxygen Species ◽  
Cancer Cell Migration ◽  
Lung Cancer Cell ◽  
Cell Migration And Invasion ◽  
Caveolin 1

High Glucose Level Induces Cardiovascular Dysplasia During Early Embryo Development

2017 ◽  
Vol 127 (09) ◽  
pp. 590-597
Author(s):  
Yi-mei Jin ◽  
Shu-zhu Zhao ◽  
Zhao-long Zhang ◽  
Yao Chen ◽  
Xin Cheng ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Reactive Oxygen Species ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
High Glucose ◽  
Reactive Oxygen ◽  
Early Embryo ◽  
Yolk Sac ◽  
Oxygen Species ◽  
Excess Reactive Oxygen Species

AbstractThe incidence of gestational diabetes mellitus (GDM) has increased dramatically amongst multiethnic population. However, how gestational diabetes mellitus damages the developing embryo is still unknown. In this study, we used yolk sac membrane (YSM) model to investigate angiogenesis in the developing chick embryo. We determined that in the presence of high glucose, it retarded the growth and extension of the embryonic vascular plexus and it also reduced the density of the vasculature in yolk sac membrane model. Using the same strategy, we used the chorioallantoic membrane (CAM) as a model to investigate the influence of high glucose on the vasculature. We established that high glucose inhibited development of the blood vessel plexus and the blood vessels formed had a narrower diameter than control vessels. Concurrent with the abnormal angiogenesis, we also examined how it impacted cardiogenesis. We determined the myocardium in the right ventricle and left atrium were significantly thicker than the control and also there was a reduction in glycogen content in cardiomyocytes. The high glucose also induced excess reactive oxygen species (ROS) production in the cardiomyocytes. We postulated that it was the excess reactive oxygen species that damaged the cardiomyocytes resulting in cardiac hyperplasia.

scholarly journals The Inhibitory Effect of Mangosteen Extract on Vascular Endothelial Growth Factor Induced Retinal Endothelial Cell Migration

2017 ◽  
Vol 35 (1) ◽  
pp. 65
Author(s):  
Kanjana Jittiporn ◽  
Wisuda Suvitayavat ◽  
Primchanien Moongkarndi ◽  
Rulth B Caldwell
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Reactive Oxygen ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Retinal Endothelial Cell ◽  
Species Production ◽  
Endothelial Growth Factor

Objective: This study aimed to determine the effect of mangosteen extract on hypoxia induced reactive oxygen species production and vascular endothelial growth factor (VEGF) induced retinal endothelial cell migration.Material and Method: This research studied bovine retinal endothelial cells. The non-toxic concentration of mangosteen extract of water soluble part was verified using trypan blue staining. The effects of mangosteen extract on hypoxia induced reactive oxygen species production and retinal endothelial cells migration were determined using 2’, 7’ dichlorodihydrofluorescein diacetate and scrape/wound assay, respectively. The mechanism of mangosteen extract on retinal endothelial cell migration was determined using western blotting. The analysis of variance was used to determine the differences among group means.Results: The concentrations of mangosteen extract at 25, 50 and 100 mg/ml were non-toxic and these concentrations were used in further experiments. Mangosteen extract at a dose of 100 mg/ml significantly attenuated hypoxia induced reactive oxygen species formation. At all doses, mangosteen extract also significantly inhibited retinal endothelial cell migration. However, the mechanism of mangosteen extract on VEGF signaling did not affect the phosphorylation of VEGF receptor 2 (VEGFR2).Conclusion: Mangosteen extract has anti-oxidant and anti-migration effects.

scholarly journals Mild Oxidative Stress Reduces NRF2 SUMOylation to Promote Kras/Lkb1/Keap1 Mutant Lung Adenocarcinoma Cell Migration and Invasion

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Jiaqian Xu ◽  
Haoyan Guo ◽  
Zhengcao Xing ◽  
Wenlong Zhang ◽  
Jianli He ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Migration ◽  
Lung Adenocarcinoma ◽  
Migration And Invasion ◽  
Related Factor ◽  
Oxygen Species ◽  
Cell Migration And Invasion ◽  
Cell Mobility ◽  
Nrf2 Activation ◽  
Signaling Process

Nuclear factor erythroid 2-related factor 2 (NRF2) is a crucial transcription factor for cell adaptation and defense against oxidative stress. NRF2 activation confers Kras/Lkb1/Keap1 (KLK) mutant tumor cells with greater resistance to oxidative insults. We previously reported that SUMOylation at lysine residue 110 is important for the ability of NRF2 to promote reactive oxygen species (ROS) clearance in hepatocellular carcinoma. In this study, we investigated whether SUMOylation is necessary for the ability of NRF2 to inhibit KLK lung adenocarcinoma (LUAD) cell migration and invasion. Our experiments showed that mild oxidative stress reduced NRF2 SUMOylation, which promoted KLK LUAD cell migration and invasion. Mechanistically, NRF2 SUMOylation increased the antioxidant ability of NRF2 and reduced cellular ROS levels, mainly by transcriptionally activating Cat in KLK LUAD cells. With reduced NRF2 SUMOylation, increased ROS acted as signaling molecules to activate the JNK/c-Jun axis, which enhanced cell mobility and cell adhesion, to promote LUAD cell migration and invasion. Taken together, the results of this study reveal a novel signaling process in which reduced NRF2 SUMOylation permits increased KLK LUAD cell migration and invasion under mild oxidative stress.

Reactive oxygen species, PKC-β1, and PKC-ζ mediate high-glucose-induced vascular endothelial growth factor expression in mesangial cells

2007 ◽  
Vol 293 (5) ◽  
pp. E1280-E1288 ◽  
Author(s):  
Ling Xia ◽  
Hong Wang ◽  
Snezana Munk ◽  
Helena Frecker ◽  
Howard J. Goldberg ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Vascular Endothelial Growth Factor ◽  
High Glucose ◽  
Mesangial Cells ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Vegf Expression ◽  
Pkc Β ◽  
Pkc Ζ ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is implicated in the development of proteinuria in diabetic nephropathy. High ambient glucose present in diabetes stimulates VEGF expression in several cell types, but the molecular mechanisms are incompletely understood. Here primary cultured rat mesangial cells served as a model to investigate the signal transduction pathways involved in high-glucose-induced VEGF expression. Exposure to high glucose (25 mM) significantly increased VEGF mRNA evaluated by real-time PCR by 3 h, VEGF cellular protein content assessed by immunoblotting or immunofluorescence within 24 h, and VEGF secretion by 24 h. High-glucose-induced VEGF expression was blocked by an antioxidant, Tempol, and antisense oligonucleotides directed against p22phox, a NADPH oxidase subunit. Inhibition of protein kinase C (PKC)-β1 with the specific pharmacological inhibitor LY-333531 or inhibition of PKC-ζ with a cell permeable specific pseudosubstrate peptide also prevented enhanced VEGF expression in high glucose. Enhanced VEGF secretion in high glucose was prevented by Tempol, PKC-β1, or PKC-ζ inhibition. In normal glucose (5.6 mM), overexpression of p22phox or constitutively active PKC-ζ enhanced VEGF expression. Hypoxia inducible factor-1α protein was significantly increased in high glucose only by 24 h, suggesting a possible contribution to high-glucose-stimulated VEGF expression at later time points. Thus reactive oxygen species generated by NADPH oxidase, and both PKC-β1 and -ζ, play important roles in high-glucose-stimulated VEGF expression and secretion by mesangial cells.

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