scholarly journals Portulaca oleraceaAmeliorates Diabetic Vascular Inflammation and Endothelial Dysfunction in db/db Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
An Sook Lee ◽  
Yun Jung Lee ◽  
So Min Lee ◽  
Jung Joo Yoon ◽  
Jin Sook Kim ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Plasma Level ◽  
Vascular Inflammation ◽  
Folk Medicine ◽  
Vascular Complications ◽  
Hdl Cholesterol ◽  
Insulin Level ◽  
Edible Plant ◽  
Diabetic Vascular Complications ◽  
Glucose Plasma

Type 2 diabetes is associated with significantly accelerated rates of micro- and macrovascular complications such as diabetic vascular inflammation and endothelial dysfunction. In the present study, we investigated the protective effect of the aqueous extract ofPortulaca oleraceaL. (AP), an edible plant used as a folk medicine, on diabetic vascular complications. The db/db mice were treated with AP (300 mg/kg/day, p.o.) for 10 weeks, and AP treatment markedly lowered blood glucose, plasma triglyceride, plasma level of LDL-cholesterol, and systolic blood pressure in diabetic db/db mice. Furthermore, AP significantly increased plasma level of HDL-cholesterol and insulin level. The impairment of ACh- and SNP-induced vascular relaxation of aortic rings were ameliorated by AP treatment in diabetic db/db mice. This study also showed that overexpression of VCAM-1, ICAM-1, E-selectin, MMP-2, and ET-1 were observed in aortic tissues of untreated db/db mice, which were significantly suppressed by treatment with AP. We also found that the insulin immunoreactivity of the pancreatic islets remarkably increased in AP treated db/db mice compared with untreated db/db mice. Taken together, AP suppresses hyperglycemia and diabetic vascular inflammation, and prevents the development of diabetic endothelial dysfunction for the development of diabetes and its vascular complications.

scholarly journals Doinseunggitang Ameliorates Endothelial Dysfunction in Diabetic Atherosclerosis

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Jung Joo Yoon ◽  
Yun Jung Lee ◽  
Ok Ju Park ◽  
So Min Lee ◽  
Yong Pyo Lee ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Vascular Inflammation ◽  
Blood Stasis ◽  
Vascular Complications ◽  
Atherosclerotic Lesion ◽  
Metabolic Parameter ◽  
Beneficial Effects ◽  
Treatment And Prevention ◽  
Diabetic Vascular Complications ◽  
Apoe Ko Mice

Atherosclerosis, a chronic and progressive disease characterized by vascular inflammation, is a leading cause of death in diabetes patients. Doinseunggitang (DYSGT), traditional prescription, has been used for promoting blood circulation to remove blood stasis. The aim of this study was to investigate the beneficial effects of DYSGT on endothelial dysfunction in diabetic atherosclerosis animal model. Apolipoprotein E knockout (ApoE KO) mice fed on a Western diet were treated with DYSGT (200 mg/kg/day). DYSGT significantly lowered blood glucose level and glucose tolerance as well as systolic blood pressure. Metabolic parameter showed that DYSGT markedly decreased triglyceride and LDL-cholesterol levels. In the thoracic aorta, the impairment of vasorelaxation response to acetylcholine and atherosclerotic lesion was attenuated by DYSGT. Furthermore, DYSGT restored the reduction of endothelial nitric oxide synthase (eNOS) expression, leading to the inhibition of intracellular adhesion molecule-1 (ICAM-1) and endothelin-1 (ET-1) expression. In conclusion, DYSGT improved the development of diabetic atherosclerosis via attenuation of the endothelial dysfunction, possibly by inhibiting ET-1, cell adhesion molecules, and lesion formation. Therefore, these results suggest that Korean traditional prescription Doinseunggitang may be useful in the treatment and prevention of diabetic vascular complications.

Icariin Attenuates High Glucose-Induced Apoptosis, Oxidative Stress, and Inflammation in Human Umbilical Venous Endothelial Cells

Planta Medica ◽  
2019 ◽  
Vol 85 (06) ◽  
pp. 473-482 ◽  
Author(s):  
Si Sun ◽  
Le Liu ◽  
Xiaojun Tian ◽  
Yanghongyun Guo ◽  
Yingkang Cao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
High Glucose ◽  
Vascular Endothelial Cells ◽  
Reactive Oxygen Species Generation ◽  
Vascular Complications ◽  
Flavonoid Glycoside ◽  
Inflammatory Factors ◽  
Diabetic Vascular Complications ◽  
Induced Apoptosis

AbstractEndothelial dysfunction is closely associated with diabetic complications. Icariin, a flavonoid glycoside isolated from the Epimedium plant species, exhibits antidiabetic properties. However, its impact on endothelial function remains poorly understood, particularly under hyperglycemia. In this study, we investigated the potential protective effect of icariin on high glucose-induced detrimental effects on vascular endothelial cells. Human umbilical venous endothelial cells were incubated in media containing 5.5 mM glucose (normal glucose) or 25 mM glucose (high glucose) in the presence or absence of 50 µM icariin for 72 h. We found that high glucose markedly induced cell apoptosis, enhanced reactive oxygen species generation, and elevated expression levels of inflammatory factors and cell adhesion molecules, which were greatly subdued by icariin supplementation. In conclusion, icariin exerted a beneficial effect on high glucose-induced endothelial dysfunction. This new finding provides a promising strategy for future treatment of diabetic vascular complications.

Relationship of Soluble RAGE and RAGE Ligands HMGB1 and EN-RAGE to Endothelial Dysfunction in Type 1 and Type 2 Diabetes Mellitus

2012 ◽  
Vol 120 (05) ◽  
pp. 277-281 ◽  
Author(s):  
J. Škrha Jr ◽  
M. Kalousová ◽  
J. Švarcová ◽  
A. Muravská ◽  
J. Kvasnička ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Advanced Glycation Endproducts ◽  
Vascular Complications ◽  
Diabetic Patients ◽  
Glycation Endproducts ◽  
Diabetic Vascular Complications ◽  
Soluble Rage

AbstractReceptor for advanced glycation endproducts (RAGE) plays the essential role in the pathogenesis of diabetic vascular complications. The aim of the study was to compare concentration of soluble RAGE and its ligands (EN-RAGE and HMGB1) with different biochemical parameters in Type 1 (T1DM) and Type 2 (T2DM) diabetes mellitus.Total number of 154 persons (45 T1DM, 68 T2DM, 41 controls) was examined and concentrations of sRAGE, EN-RAGE and HMGB1 were measured and compared to diabetes control, albuminuria, cell adhesion molecules and metalloproteinases (MMPs).Mean serum sRAGE concentration was higher in T1DM as compared to controls (1137±532 ng/l vs. 824±309 ng/l, p<0.01). Similarly, EN-RAGE was significantly higher in both diabetic groups (p<0.001) and HMGB1 concentrations were elevated in T2DM patients (p<0.01). Significant relationship was found between MMP9 and HMGB1 and EN-RAGE in diabetic patients. Inverse relationship was observed between MMP2 and MMP9 in both types of diabetic patients (r= − 0.602, p<0.002 and r= − 0.771, p<0.001). Significant positive correlation was found between sRAGE and ICAM-1, VCAM-1 or vWF (p<0.01 to p<0.001).We conclude that serum sRAGE and RAGE ligands concentrations reflect endothelial dysfunction developing in diabetes.

scholarly journals Epigenetic regulation in diabetic vascular complications

2019 ◽  
Vol 63 (4) ◽  
pp. R103-R115 ◽  
Author(s):  
Jiayu Jin ◽  
Xinhong Wang ◽  
Xiuling Zhi ◽  
Dan Meng
Keyword(s):  
Endothelial Dysfunction ◽  
Epigenetic Regulation ◽  
Epigenetic Modification ◽  
Vascular Complications ◽  
Integrated System ◽  
Metabolic Memory ◽  
Diabetic Patients ◽  
Epigenetic Alterations ◽  
Diabetic Vascular Complications ◽  
Legacy Effect

Cardiovascular disease (CVD), the main complication of diabetes mellitus (DM), accounts for a high percentage of mortality in diabetic patients. Endothelial dysfunction is a major causative event in the pathogenesis of diabetes-related vascular disease and the earliest symptom of vascular injury. Epigenetic modification plays a key role in the initiation, maintenance, and progression of both endothelial dysfunction and diabetes. Epigenetic alterations respond to the environment and mediate the ‘legacy effect’ of uncontrolled hyperglycaemia early in the disease despite thorough glycaemic control in a phenomenon called metabolic memory. Therefore, an understanding of the integrated system of different epigenetic mechanisms in DM and its vascular complications is urgently needed. This review summarizes aberrant epigenetic regulation under diabetic conditions, including histone modifications, DNA methylation, and non-coding RNAs (ncRNAs). Understanding the connections between these processes and DM may reveal a novel potential therapeutic target for diabetic vascular complications.

scholarly journals The Contribution of Endothelial Dysfunction in Systemic Injury Subsequent to SARS-Cov-2 Infection

2020 ◽  
Vol 21 (23) ◽  
pp. 9309
Author(s):  
Jessica Maiuolo ◽  
Rocco Mollace ◽  
Micaela Gliozzi ◽  
Vincenzo Musolino ◽  
Cristina Carresi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Blood Vessels ◽  
Molecular Mechanisms ◽  
Vascular Dysfunction ◽  
Vascular Inflammation ◽  
Vascular Complications ◽  
Therapeutic Interventions ◽  
The Impact

SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) infection is associated, alongside with lung infection and respiratory disease, to cardiovascular dysfunction that occurs at any stage of the disease. This includes ischemic heart disease, arrhythmias, and cardiomyopathies. The common pathophysiological link between SARS-CoV-2 infection and the cardiovascular events is represented by coagulation abnormalities and disruption of factors released by endothelial cells, which contribute in maintaining the blood vessels into an anti-thrombotic state. Thus, early alteration of the functionality of endothelial cells, which may be found soon after SARS-CoV-2 infection, seems to represent the major target of a SARS CoV-2 disease state and accounts for the systemic vascular dysfunction that leads to a detrimental effect in terms of hospitalization and death accompanying the disease. In particular, the molecular interaction of SARS-CoV-2 with the ACE2 receptor located in the endothelial cell surface, either at the pulmonary and systemic level, leads to early impairment of endothelial function, which, in turn, is followed by vascular inflammation and thrombosis of peripheral blood vessels. This highlights systemic hypoxia and further aggravates the vicious circle that compromises the development of the disease, leading to irreversible tissue damage and death of people with SARS CoV-2 infection. The review aims to assess some recent advances to define the crucial role of endothelial dysfunction in the pathogenesis of vascular complications accompanying SARS-CoV-2 infection. In particular, the molecular mechanisms associated with the interaction of SARS CoV-2 with the ACE2 receptor located on the endothelial cells are highlighted to support its role in compromising endothelial cell functionality. Finally, the consequences of endothelial dysfunction in enhancing pro-inflammatory and pro-thrombotic effects of SARS-CoV-2 infection are assessed in order to identify early therapeutic interventions able to reduce the impact of the disease in high-risk patients.

scholarly journals ERK-containing microparticles from a diabetic mouse induce endothelial dysfunction

2019 ◽  
Vol 241 (3) ◽  
pp. 221-233 ◽  
Author(s):  
Kumiko Taguchi ◽  
Haruka Narimatsu ◽  
Takayuki Matsumoto ◽  
Tsuneo Kobayashi
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Vascular Complications ◽  
Diabetic Mouse ◽  
Diabetic Rats ◽  
Enzyme Linked Immunosorbent Assay ◽  
Diabetic Mice ◽  
Diabetic Vascular Complications ◽  
Underlying Mechanisms

Endothelial dysfunction is a hallmark of diabetic vascular complications. Microparticles (MPs) are small vesicles shed from the surface of blood and vascular cells that act as stimuli and during apoptosis. Circulating MPs of diabetic rats have been shown to induce endothelial dysfunction. However, the underlying mechanisms require further study. In this study, we investigated how MPs from diabetic mice affect endothelial function. MPs were collected from streptozotocin-induced diabetic mice and Institute of Cancer Research (ICR) mice as controls. The levels of MPs were assessed and characterized by flow cytometry, enzyme-linked immunosorbent assay and dot blotting. Normal mice aortas were incubated with MPs and expressions of enzymes and vascular relaxation were analyzed. We found that (1) circulating MPs level increased in diabetic mice; (2) MPs impaired endothelial-dependent relaxation in mice aorta, but diabetic mice-derived MPs (diabetes mellitus (DM) MPs) were easier to attach to the endothelial cells than were control MPs; (3) DM MPs had more extracellular signal-regulated kinase (ERK)1/2 than did control mice-derived MPs, and they induced ERK1/2 activation in mice aortas; (4) DM MPs decreased endothelial nitric oxide synthase (eNOS) in mice aortas, and eNOS was emitted from endothelial cells to blood in the shape of endothelial MPs. DM MPs significantly altered endothelial function by activation of ERK1/2, which might provide a therapeutic target for diabetic vascular complications.

scholarly journals Dyslipidemia’s influence on the secretion ovarian’s steroids in female mice

2021 ◽  
Vol 10 (13) ◽  
pp. e298101321369
Author(s):  
Juliana Maganha Abreu ◽  
Gérsika Bitencourt Santos ◽  
Maria das Graças de Souza Carvalho ◽  
Juliana Marques Mencarelli ◽  
Bruna Rayanne Moreira Cândido ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Plasma Levels ◽  
High Fat Diet ◽  
Hdl Cholesterol ◽  
Insulin Level ◽  
Standard Diet ◽  
High Fat ◽  
Wild Female ◽  
Female Mice ◽  
Glucose Plasma

Introduction: The synthesis ovarian’s steroids is a process thats depends on the supply of cholesterol. Objective: to evaluate the influence of dyslipidemia on the secretion ovarian’s steroids. Methodology: wild female mice were used (C57BL6) and LDL (LDLR-/-), which they were separated into 4 groups (n = 10): WTS: fed a standard diet; WTHL: fed a high-fat diet; KOS: fed a standard diet; KOHL: fed a high-fat diet. After 60 days, the estrous cycle was analyzed and after anesthetized, blood was collected for the to assess the lipid profile, glucose, plasma insulin level and HOMA index was calculated. In addition, plasma levels of C-reactive protein, estrogen and progesterone were determined. Results: The hyperlipidic diet in both the WTHL and the KOHL group generated hypercholesterolemia when compared to the WTS and KOS, respectively, with a decrease in HDLc, associated with an increase in CRP levels. Severe hypercholesterolemia in the KOHL group generated insulin resistance, marked by an increase in HOMAir. Food hypercholesterolemia in the WTHL group, food and genetics in the KOHL group, compared to their WTS and KOS controls, was definitive in reducing plasma levels of estrogen and progesterone. The genetic hypercholesterolemia associated with insulin resistance observed in the KOS and KOHL groups reduced the levels of progesterone, this reduction being more severe in the KOHL group, which had the highest HOMAir. Conclusion: dyslipidemia affected ovarian steroidogenesis in mice by means of oxidative stress, inflammation and insulin resistance and / or by decreasing HDL cholesterol levels.

scholarly journals The Contribution of Endothelial Dysfunction in Systemic Injury Subsequent to SARS-Cov-2 Infection

2020 ◽  
Author(s):  
Jessica Maiuolo ◽  
Rocco Mollace ◽  
Micaela Gliozzi ◽  
Vincenzo Musolino ◽  
Cristina Carresi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Blood Vessels ◽  
Molecular Mechanisms ◽  
Vascular Dysfunction ◽  
Vascular Inflammation ◽  
Vascular Complications ◽  
Therapeutic Interventions ◽  
The Impact

Abstract: SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) infection is associated, alongside with lung infection and respiratory disease, to cardiovascular dysfunction that occurs at any stage of the disease. This includes ischemic heart disease, arrhythmias, and cardiomyopathies. The common pathophysiological link between SARS-CoV-2 infection and the cardiovascular events is represented by coagulation abnormalities and disruption of factors released by endothelial cells which contribute in maintaining the blood vessels into an anti-thrombotic state. Thus, early alteration of the functionality of endothelial cells, which may be found soon after SARS-CoV-2 infection, seems to represent the major target of SARS CoV-2 disease state and accounts for the systemic vascular dysfunction that leads to detrimental effect in terms of hospitalization and death accompanying the disease. In particular, the molecular interaction of SARS-CoV-2 with ACE2 receptor located in endothelial cell surface, either at the pulmonary and systemic level, leads to early impairment of endothelial function which, in turn, is followed by vascular inflammation and thrombosis of peripheral blood vessels. This highlights systemic hypoxia and further aggravates the vicious circle that compromises the development of the disease leading to irreversible tissue damage and death of patients with SARS CoV-2 infection. The review aims to assess some recent advances to define the crucial role of endothelial dysfunction in the pathogenesis of vascular complications accompanying SARS-CoV-2 infection. In particular, the molecular mechanisms associated to the interaction of SARS CoV-2 with ACE2 receptor located on the endothelial cells are highlighted to support its role in compromising endothelial cell functionality. Finally, the consequences of endothelial dysfunction in enhancing pro-inflammatory and pro-thrombotic effects of SARS-CoV-2 infection are assessed in order to identify early therapeutic interventions able to reduce the impact of the disease in high-risk patients.

scholarly journals Roles of Endovascular Calyx Related Enzymes in Endothelial Dysfunction and Diabetic Vascular Complications

2020 ◽  
Vol 11 ◽  
Author(s):  
Zhi Li ◽  
Ning Wu ◽  
Jing Wang ◽  
Quanbin Zhang
Keyword(s):  
Quality Of Life ◽  
Hyaluronic Acid ◽  
Endothelial Dysfunction ◽  
Vascular Complications ◽  
Diabetic Patients ◽  
Complications Of Diabetes ◽  
Diabetic Vascular Complications ◽  
Hyaluronic Acid Synthase ◽  
The Relationship

In recent years, the number of diabetic patients has rapidly increased. Diabetic vascular complications seriously affect people’s quality of life. Studies found that endothelial dysfunction precedes the vascular complications of diabetes. Endothelial dysfunction is related to glycocalyx degradation on the surface of blood vessels. Heparanase (HPSE), matrix metalloproteinase (MMP), hyaluronidase (HYAL), hyaluronic acid synthase (HAS), and neuraminidase (NEU) are related to glycocalyx degradation. Therefore, we reviewed the relationship between endothelial dysfunction and the vascular complications of diabetes from the perspective of enzymes.

Abstract P034: Endothelin-1 Overexpression Exaggerates Diabetes-induced Endothelial Dysfunction by Altering Oxidative Stress Balance

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Noureddine Idris Khodja ◽  
Sofiane Ouerd ◽  
Muhammad Oneeb Rehman Mian ◽  
Jordan Gornitsky ◽  
Tlili Barhoumi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Vascular Complications ◽  
Superoxide Production ◽  
Superoxide Dismutase 1 ◽  
Mitochondrial Oxidative Stress ◽  
Mitochondrial Superoxide ◽  
Glucose Plasma ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Objective: Increased endothelin (ET)-1 expression has been shown to cause endothelial dysfunction.Plasma ET-1 is increased in patients with diabetes.Since endothelial dysfunction often precedes vascular complications in diabetes, we sought to determine whether ET-1 contributes to diabetes-induced endothelial dysfunction. We hypothesized that overexpression of ET-1 in the endotheliumwill exaggerate diabetes-induced endothelial dysfunction. Method: Diabetes was induced by streptozotocin treatment (STZ, 55 mg/kg/day, ip) for 5 days in 6weekold male wild-type (WT) mice and in mice overexpressinghuman ET-1 restricted to the endothelium (eET-1). Mice were studied 14 weeks later. Blood glucose,plasma ET-1 levels, mesenteric artery (MA) reactivity, mitochondrial superoxide production in aorta and endothelial nitric oxide synthase (Nos3), superoxide dismutase 1 (Sod1) and 2 (Sod2) mRNA expression in MA were determined. Results: STZ-induced diabetes was confirmed by increased glycemia in WT(27.6±1.5 vs 10.7±1.1 μM, P<0.001)and eET-1 (23.2±1.0 vs 8.4±0.3 μM, P<0.001).Plasma ET-1 was increased in vehicle- (15.9±4.6 vs 0.6±0.04pg/mL, P<0.05) and STZ-treatedeET-1 (4.9±0.6 vs 0.8±0.1 pg/mL, P<0.05) compared to respective WT controls.Diabetes caused a reduction in vasodilatory responses to acetylcholine in WT (60.9±6.4% vs 83.9±3.4%,P<0.05), which was exaggerated in eET-1(48.6±5.1% vs 81.5±5.2% P<0.05). Mitochondrial superoxide production was increased by diabetes in WT (38.0±4.3 vs 21.6±2.3 RFU/μm2,P<0.05)and further augmented in eET-1 (49.8±1.7 RFU/μm2P<0.05).Nos3 expression was increased in vehicle-treatedeET-1 compared to WT(1.43±0.19 vs 1.00±0.10, P<0.05).Diabetes reduced Nos3 expression in eET-1 (0.75±0.08, P<0.05) but not in WT(1.08±0.09).Diabetes caused an increase in Sod1(1.52±0.17 vs 1.00±0.03, P<0.05) and Sod2 (1.32±0.17 vs 1.00±0.02, P<0.05) expression in WT (P<0.05) but not in eET-1. Conclusions: Increased levels of ET-1 exaggerate diabetes-induced endothelial dysfunction. This may be caused by a decrease in Nos3 expression, an increase in mitochondrial oxidative stress and a decrease in antioxidant capacity.

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