Trivalent Chromium Supplementation Inhibits Oxidative Stress, Protein Glycosylation, and Vascular Inflammation in High Glucose-Exposed Human Erythrocytes and Monocytes

2007 ◽  
pp. 301-313
Author(s):  
Sushil Jain
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Vascular Inflammation ◽  
Stress Protein ◽  
Trivalent Chromium ◽  
Human Erythrocytes ◽  
Protein Glycosylation

Abstract 14746: Dynamic SIRTUIN1-modulated Lysine Acetylation of P66shc Governs Vascular Endothelial Oxidative Stress and Dysfunction of Diabetes

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Santosh Kumar ◽  
Young Rae Kim ◽  
Ajit Vikram ◽  
Asma Naqvi ◽  
Ajay Kumar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Vascular Dysfunction ◽  
Stress Protein ◽  
Lysine Acetylation ◽  
Vascular Endothelial ◽  
Endothelium Dysfunction ◽  
Lysine Deacetylase ◽  
Oxidative Function

The SIRTUIN1 lysine deacetylase (SIRT1) ameliorates diabetic vascular dysfunction by epigenetically suppressing endothelial expression of the oxidative stress protein p66shc. However, whether SIRT1 modulates the oxidative function of p66shc by directly targeting it for lysine deacetylation is not known. Here we show that the oxidative function of p66shc is dynamically modulated by lysine acetylation. Mass spectroscopy identified lysine 81 in the unique CH2 domain of p66shc as the residue targeted by SIRT1. High glucose and SIRT1 knockdown stimulates acetylation of lysine 81 of endothelial p66shc. Compared to WT p66shc, non-acetylatable (K81R) p66shc is significantly handicapped in promoting endothelial hydrogen peroxide production stimulated by high glucose. Compared to WT p66shc, K81R p66shc is also less prone to serine 36 phosphorylation by high glucose, which is essential for the oxidative function of p66shc. Moreover, in contrast to WT p66shc which worsens endothelial dysfunction, expression of K81R p66shc does not impair endothelial function in wild type mice and rescues endothelium dysfunction of diabetic db+/db+ mouse aortas . These findings show that lysine 81 acetylation promotes the oxidative role of p66shc in hyperglycemic conditions, and is essential for p66shc-mediated endothelial dysfunction.

Trivalent Chromium Inhibits Protein Glycosylation and Lipid Peroxidation in High Glucose-Treated Erythrocytes

2006 ◽  
Vol 8 (1-2) ◽  
pp. 238-241 ◽  
Author(s):  
Sushil K. Jain ◽  
Parag Patel ◽  
Kimberly Rogier ◽  
Sumati K. Jain
Keyword(s):  
Lipid Peroxidation ◽  
High Glucose ◽  
Trivalent Chromium ◽  
Protein Glycosylation

scholarly journals Effects of Three Kinds of Curcuminoids on Anti-Oxidative System and Membrane Deformation of Human Peripheral Blood Erythrocytes in High Glucose Levels

2015 ◽  
Vol 35 (2) ◽  
pp. 789-802 ◽  
Author(s):  
Wei Yang ◽  
Juan Fu ◽  
Miao Yu ◽  
Di Wang ◽  
Ying Rong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
High Glucose ◽  
Human Peripheral Blood ◽  
Human Erythrocytes ◽  
Protein Glycation ◽  
Bioactive Constituents ◽  
Blood Samples ◽  
Glucose Levels ◽  
Stress Damage

Background/Aims: Curcuminoids are the main bioactive constituents of the rhizome of turmeric. Erythrocytes lesions in diabetes are probably related to hyperglycemia and protein glycation. It has been reported that curcumin prevent lipid peroxidation. However, reports on the effects of demethoxycurcumin and bis-demethoxycurcumin on human erythrocytes at high glucose levels are scarce. Our aim is to investigate the effect of curcuminoids on oxidative stress and membrane of erythrocytes exposed to hyperglycemic condition. Methods: In this study, the different blood samples were treated with two doses of glucose (10 or 30 mM) to mimic hyperglycemia in the presence or absence of three kinds of curcuminoids (5 or 10 μM) in a medium at 37 °C for 24 h (Each experiment consists of 20 blood samples from 10 male and 10 female volunteers). The malondialdehyde was checked by HPLC, antioxidase (GSH and GSSG) were measured by LC/MS, SOD was checked by WST-1 kit, morphology and phospholipid symmetry were detected by flow cytometry, confocal scanning microscope and scanning electron microscope. Results: The results illustrated that all three curcuminoids reduce oxidative stress damage on the membrane and maintain a better profile for erythrocytes. Furthermore, three curcuminoids had benefit effects on antioxidase. Conclusion: The three kinds of curcuminoids supplementation may prevent lipid peroxidation at different intensity and membrane dysfunction of human erythrocytes in hyperglycemia.

scholarly journals Extracellular Hsp90α is a Potential Serum Predictor of Atherosclerosis in type 2 Diabetes

2021 ◽  
Author(s):  
Xinyi Ding ◽  
Chuzhen Meng ◽  
Hangming Dong ◽  
Shili Zhang ◽  
Hui Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Vascular Disease ◽  
High Glucose ◽  
Cell Injury ◽  
Vascular Inflammation ◽  
Diabetic Patients ◽  
Monocyte Migration ◽  
The Relationship

Abstract Background: Atherosclerosis is the main pathological change in diabetic angiopathy, and vascular inflammation plays an important role in early atherosclerosis. Heat shock protein 90, a cellular molecular chaperone, was recently determined to be secreted extracellularly, but the specific mechanism remains unclear. This study explored the relationship between Hsp90 and diabetic peripheral artery disease through serological analyses of different groups of diabetic patients and investigated the relationship between extracellular Hsp90α and vascular inflammation at the cellular level.Methods: Seventy-seven selected patients were divided into three groups. The relationships among serum Hsp90, oxidative stress indexes and patient outcomes and the correlations among the indexes were analysed. An oxidative stress endothelial injury model was established under high glucose in vitro to explore the role of eHsp90 release in atherosclerosis progression.Results: Serum Hsp90 and MDA levels tended to increase in different groups with peripheral vascular disease aggravation. Hsp90α was correlated with MDA to some extent and was predictive. In vitro, high glucose and low H2O2 treatment increased extracellular Hsp90 secretion, and endothelial cell conditioned medium and recombinant human Hsp90α increased monocyte migration (P<0.05).Conclusions: Extracellular Hsp90α participates in endothelial cell injury in diabetic vascular disease and initiates the inflammatory response by promoting monocyte migration.Trial registration: NCT04787770, ClinicalTrials.gov, Registered 9 March, 2021 - Prospective registered

scholarly journals Sanguis draconis, a Dragon’s Blood Resin, Attenuates High Glucose-Induced Oxidative Stress and Endothelial Dysfunction in Human Umbilical Vein Endothelial Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Yi Chang ◽  
Ting-Chen Chang ◽  
Jie-Jen Lee ◽  
Nen-Chung Chang ◽  
Yung-Kai Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Umbilical Vein ◽  
Vascular Inflammation ◽  
Dependent Manner ◽  
Dragon’S Blood ◽  
Umbilical Vein Endothelial Cells ◽  
Parp 1

Hyperglycaemia, a characteristic feature of diabetes mellitus, induces endothelial dysfunction and vascular complications by limiting the proliferative potential of these cells. Here we aimed to investigate the effect of an ethanolic extract ofSanguis draconis(SD), a kind of dragon’s blood resin that is obtained fromDaemonorops draco(Palmae), on human umbilical vein endothelial cells (HUVEC) under high-glucose (HG) stimulation and its underlying mechanism. Concentration-dependent (0–50 μg/mL) assessment of cell viability showed that SD does not affect cell viability with a similar trend up to 48 h. Remarkably, SD (10–50 μg/mL) significantly attenuated the high-glucose (25 and 50 mM) induced cell toxicity in a concentration-dependent manner. SD inhibited high glucose-induced nitrite (NO) and lipid peroxidation (MDA) production and reactive oxygen species (ROS) formation in HUVEC. Western blot analysis revealed that SD treatments abolished HG-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK 1/2), nuclear transcription factor,κB (NF-κB), VCAM-1, and E-selectin, and it also blocked the breakdown of PARP-116 kDa protein in a dose-dependent manner. Furthermore, we found that SD increased the expression of Bcl-2 and decreased Bax protein expression in HG-stimulated HUVEC. Thus, these results of this study demonstrate for the first time that SD inhibits glucose induced oxidative stress and vascular inflammation in HUVEC by inhibiting the ERK/NF-κB/PARP-1/Bax signaling cascade followed by suppressing the activation of VCAM-1 and E-selectin. These data suggest that SD may have a therapeutic potential in vascular inflammation due to the decreased levels of oxidative stress, apoptosis, and PARP-1 activation.

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