scholarly journals Possible Mechanisms of Endothelioproteсtion 4-Hydroxy-3,5-DiTretbutyl Cinnamic Acid in the Cerebral Ischemia in Experiment

2017 ◽  
Vol 9 (03) ◽  
Author(s):  
D. I. Pozdnyakov ◽  
A. V. Voronkov ◽  
D. S. Zolotych
Keyword(s):  
Cerebral Ischemia ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Brain Ischemia ◽  
Cinnamic Acid ◽  
Asymmetric Dimethylarginine ◽  
Mechanisms Of Action ◽  
Thioctic Acid ◽  
Experimental Conditions ◽  
Endothelium Dysfunction

Conducted research devoted to the study of potential mechanisms of action implementation endotelioproteсtion 4-hydroxy- 3,5-di-tretbutyl cinnamic acid in experimental conditions simulated cerebral ischemia in rats. The research found that the cerebral ischemia in rats is accompanied by the development of endothelial dysfunction, expressed in increasing the concentration of asymmetric dimethylarginine, nNOS, iNOS and PKC, as well as reducing the concentration of eNOS. Introduction of sulodexide (to a greater extent compared with thioctic acid and mexidol restores endothelial function in conditions of brain ischemia in rats. The use of 4-hydroxy-3,5-di-tretbutyl cinnamic acid helped reduce the concentration of ADMA, nNOS, iNOS and PKC on 83.9% (p >0.05), 60.6% (p >0.05), 61. 9% (p >0.05), 108.6% (p >0.05), respectively, as well as improve the content of eNOS at 114.2% (p >0.05), thereby contributing to the correction that has developed in conditions cerebral ischemia, endothelium dysfunction

scholarly journals Paracrine Shear-Stress-Dependent Signaling from Endothelial Cells Affects Downstream Endothelial Function and Inflammation

2021 ◽  
Vol 22 (24) ◽  
pp. 13300
Author(s):  
Fabio Bertani ◽  
Dalila Di Francesco ◽  
Maria Dolores Corrado ◽  
Maria Talmon ◽  
Luigia Grazia Fresu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Conditioned Media ◽  
Coronary Microvascular Dysfunction ◽  
Experimental Conditions ◽  
Low Shear Stress ◽  
Stress Dependent ◽  
Low Shear

Cardiovascular diseases (CVDs), mainly ischemic heart disease (IHD) and stroke, are the leading cause of global mortality and major contributors to disability worldwide. Despite their heterogeneity, almost all CVDs share a common feature: the endothelial dysfunction. This is defined as a loss of functionality in terms of anti-inflammatory, anti-thrombotic and vasodilatory abilities of endothelial cells (ECs). Endothelial function is greatly ensured by the mechanotransduction of shear forces, namely, endothelial wall shear stress (WSS). Low WSS is associated with endothelial dysfunction, representing the primary cause of atherosclerotic plaque formation and an important factor in plaque progression and remodeling. In this work, the role of factors released by ECs subjected to different magnitudes of shear stress driving the functionality of downstream endothelium has been evaluated. By means of a microfluidic system, HUVEC monolayers have been subjected to shear stress and the conditioned media collected to be used for the subsequent static culture. The results demonstrate that conditioned media retrieved from low shear stress experimental conditions (LSS-CM) induce the downregulation of endothelial nitric oxide synthase (eNOS) expression while upregulating peripheral blood mononuclear cell (PBMC) adhesion by means of higher levels of adhesion molecules such as E-selectin and ICAM-1. Moreover, LSS-CM demonstrated a significant angiogenic ability comparable to the inflammatory control media (TNFα-CM); thus, it is likely related to tissue suffering. We can therefore suggest that ECs stimulated at low shear stress (LSS) magnitudes are possibly involved in the paracrine induction of peripheral endothelial dysfunction, opening interesting insights into the pathogenetic mechanisms of coronary microvascular dysfunction.

DISTURBANCES OF ANTITHROMBOTIC VASCULAR ENDOTHELIAL FUNCTION AND SOME PLASMA HEMOSTATIC PARAMETERS AT FOCAL CEREBRAL ISCHEMIA AND THEIR CORRECTION BY 4-HYDROXY-3,5-DITRETBUTYL CINNAMIC ACID

2017 ◽  
Author(s):  
А. Воронков ◽  
Д. Поздняков
Keyword(s):  
Platelet Aggregation ◽  
Cerebral Ischemia ◽  
Cinnamic Acid ◽  
Vascular Endothelium ◽  
Focal Cerebral Ischemia ◽  
Male Rats ◽  
Vascular Endothelial ◽  
Thioctic Acid ◽  
Vascular Endothelial Function ◽  
Aggregation Activity

Введение. Рост числа случаев ишемического инсульта (ИИ) в РФ диктует необходимость поиска путей снижения заболеваемости, а также уменьшения числа случаев летального исхода. Одним из таких направлений можно считать рациональное фармакологическое воздействие на основные звенья патогенеза повреждения головного мозга при ИИ. Цель исследования. Оценить степень изменения антитромботической функции сосудистого эндотелия на фоне фокальной ишемии головного мозга, а также способность 4-гидрокси-3,5-дитретбутил коричной кислоты препятствовать развитию данных изменений. Материалы и методы. В эксперименте на 60 крысах-самцах линии Wistar), разделенных на 6 равных экспериментальных групп (nH=H10), исследовали влияние 4-гидрокси-3,5-дитретбутил коричной кислоты на антитромботическую функцию эндотелия и некоторые показатели плазменного гемостаза на фоне фокальной ишемии головного мозга. Результаты. Установлено, что введение 4-гидрокси-3,5-дитретбутил коричной кислоты в дозе 100 мг/кг на фоне фокальной ишемии головного мозга способствовало снижению агрегационной активности тромбоцитов: отмечено уменьшение степени (на 37,7%) и скорости (150,3%) агрегации тромбоцитов по сравнению с животными, не получавшими фармакологическую поддержку, а также восстановление активности свертывающей и противосвертывающей систем крови. Заключение. По величине фармакологического эффекта изучаемое соединение превосходило мексидол и тиоктовую кислоту и не уступало сулодексиду. Introduction. Increasing number of ischemic stroke (IS) cases in Russian Federation requires the necessity to find ways for reducing morbidity and death incidence. Balanced pharmacological infl uence on the main pathogenesis links of brain damage at IS can be one of opportunities. The aim: to assess changes in antithrombotic function of vascular endothelium at focal cerebral ischemia and also the ability of 4-hydroxy-3,5-di-tert-butyl cinnamic acid to prevent the development of these changes. Materials and methods. The effect of 4-hydroxy-3,5-ditretbutyl cinnamic acid on endothelial antithrombotic function and some plasma hemostatic parameters at focal cerebral ischemia was studied in experiment on 60 male rats (Wistar line) divided into 6 equal experimental groups (nH=H10). Results. We found that the administration of 4-hydroxy-3,5-ditretbutyl cinnamic acid (100 mg/kg) at focal cerebral ischemia decreased platelet aggregation activity: we registered the reduction in degree (by 37,7%) and speed (150,3%) of platelet aggregation compared to animals who did not receive pharmacological support, and also the restoration of blood coagulation and anticoagulation activities. Conclusion. Pharmacological effect of studied compound exceeded mexidol and thioctic acid actions and was similar to sulodexide influence.

scholarly journals ENDOTHELIAL DYSFUNCTION IN MEN - A CLINICAL VIEW

2014 ◽  
Vol 13 (5) ◽  
pp. 169-178
Author(s):  
I. A. Khripun ◽  
Z. R. Gtisova ◽  
H. S. Ibishev ◽  
A. S. Sultanmuradova ◽  
S. V. Vorobiev ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Vascular Endothelium ◽  
Late Onset ◽  
Hormone Replacement ◽  
Mechanisms Of Action ◽  
Clinical Use ◽  
Testosterone Deficiency ◽  
Late Onset Hypogonadism ◽  
Instrumental Methods

Endothelial dysfunction is an early marker for the development and progression of cardiovascular diseases. Scientific studies in recent years have shown the necessity to study the endothelial function in different groups of patients in clinical practice. This article is focused on the possibilities and perspectives for clinical use of laboratory and instrumental methods for the study of endothelial function. One of the factors causing the development of vascular disease in men is testosterone deficiency. The review highlights the most important mechanisms of action of sex hormones on the vascular endothelium and its function in men. The data about the effects of hormone replacement therapy with testosterone on endothelial function in patients with late onset hypogonadism were critically analyzed.

Coronary Artery Disease and Endothelial Dysfunction: Novel Diagnostic and Therapeutic Approaches

2020 ◽  
Vol 27 (7) ◽  
pp. 1052-1080 ◽  
Author(s):  
Evangelos Oikonomou ◽  
Gerasimos Siasos ◽  
Vasiliki Tsigkou ◽  
Evanthia Bletsa ◽  
Maria-Evi Panoilia ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Stable Coronary Artery Disease ◽  
Therapeutic Interventions ◽  
Therapeutic Approaches ◽  
Cardiovascular Prognosis ◽  
Ultrasound Evaluation ◽  
Artery Disease

Coronary artery disease is the leading cause of morbidity and mortality worldwide. The most common pathophysiologic substrate is atherosclerosis which is an inflammatory procedure that starts at childhood and develops throughout life. Endothelial dysfunction is associated with the initiation and progression of atherosclerosis and is characterized by the impaired production of nitric oxide. In general, endothelial dysfunction is linked to poor cardiovascular prognosis and different methods, both invasive and non-invasive, have been developed for its evaluation. Ultrasound evaluation of flow mediated dilatation of the branchial artery is the most commonly used method to assessed endothelial function while intracoronary administration of vasoactive agents may be also be used to test directly endothelial properties of the coronary vasculature. Endothelial dysfunction has also been the subject of therapeutic interventions. This review article summarizes the knowledge about evaluation of endothelial function in acute coronary syndromes and stable coronary artery disease and demonstrates the current therapeutic approaches against endothelial dysfunction.

Therapeutic Potential of Phosphodiesterase Inhibitors for Endothelial Dysfunction- Related Diseases

2020 ◽  
Vol 26 (30) ◽  
pp. 3633-3651 ◽  
Author(s):  
Javier Blanco-Rivero ◽  
Fabiano E. Xavier
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Therapeutic Potential ◽  
Treatment Strategies ◽  
Phosphodiesterase Inhibitors ◽  
Developed Countries ◽  
Major Health Problem ◽  
Pde Inhibitors ◽  
Pharmaceutical Industries

Cardiovascular diseases (CVD) are considered a major health problem worldwide, being the main cause of mortality in developing and developed countries. Endothelial dysfunction, characterized by a decline in nitric oxide production and/or bioavailability, increased oxidative stress, decreased prostacyclin levels, and a reduction of endothelium-derived hyperpolarizing factor is considered an important prognostic indicator of various CVD. Changes in cyclic nucleotides production and/ or signalling, such as guanosine 3', 5'-monophosphate (cGMP) and adenosine 3', 5'-monophosphate (cAMP), also accompany many vascular disorders that course with altered endothelial function. Phosphodiesterases (PDE) are metallophosphohydrolases that catalyse cAMP and cGMP hydrolysis, thereby terminating the cyclic nucleotide-dependent signalling. The development of drugs that selectively block the activity of specific PDE families remains of great interest to the research, clinical and pharmaceutical industries. In the present review, we will discuss the effects of PDE inhibitors on CVD related to altered endothelial function, such as atherosclerosis, diabetes mellitus, arterial hypertension, stroke, aging and cirrhosis. Multiple evidences suggest that PDEs inhibition represents an attractive medical approach for the treatment of endothelial dysfunction-related diseases. Selective PDE inhibitors, especially PDE3 and PDE5 inhibitors are proposed to increase vascular NO levels by increasing antioxidant status or endothelial nitric oxide synthase expression and activation and to improve the morphological architecture of the endothelial surface. Thereby, selective PDE inhibitors can improve the endothelial function in various CVD, increasing the evidence that these drugs are potential treatment strategies for vascular dysfunction and reinforcing their potential role as an adjuvant in the pharmacotherapy of CVD.

Magnesium intake, insulin resistance and markers of endothelial function among women

2021 ◽  
pp. 1-9
Author(s):  
Narges Ghorbani Bavani ◽  
Parvane Saneei ◽  
Ammar Hassanzadeh Keshteli ◽  
Ahmadreza Yazdannik ◽  
Ebrahim Falahi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Adhesion Molecule ◽  
Cell Function ◽  
Intercellular Adhesion Molecule ◽  
Model Assessment ◽  
Serum Concentrations ◽  
Homeostasis Model Assessment

Abstract Objective: We investigated the association of dietary Mg intake with insulin resistance and markers of endothelial function among Iranian women. Design: A cross-sectional study. Setting: Usual dietary intakes were assessed using a validated FFQ. Dietary Mg intake was calculated by summing up the amount of Mg in all foods. A fasting blood sample was taken to measure serum concentrations of glycemic indices (fasting plasma glucose and insulin) and endothelial function markers (E-selectin, soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1). Insulin resistance and sensitivity were estimated using the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR), Homeostasis Model Assessment β-cell function (HOMA-β) and quantitative insulin sensitivity check index (QUICKI). Participants: Iranian female nurses (n 345) selected by a multistage cluster random sampling method. Results: The Mg intake across energy-adjusted quartiles was 205 (se 7), 221·4 (se 8), 254·3 (se 7) and 355·2 (se 9) mg/d, respectively. After adjustments for potential confounders, QUICKI level was significantly different across quartiles of Mg intake (Q1: 0·34 (se 0·02), Q2: 0·36 (se 0·01), Q3: 0·40 (se 0·01), and Q4: 0·39 (se 0·02), P = 0·02); however, this association disappeared after considering markers of endothelial function, indicating that this relation might be mediated through endothelial dysfunction. After controlling for all potential confounders, Mg intake was inversely, but not significantly, associated with serum concentrations of sICAM (Q1: 239 (se 17), Q2: 214 (se 12), Q3: 196 (se 12), and Q4: 195 (se 17), P = 0·29). There was no other significant association between dietary Mg intake and other indicators of glucose homoeostasis or endothelial markers. Conclusions: Higher dietary Mg intake was associated with better insulin sensitivity in Iranian females. This linkage was mediated through reduced endothelial dysfunction.

scholarly journals Comparison of biomarkers of endothelial dysfunction and microvascular endothelial function in patients with primary aldosteronism and essential hypertension

2021 ◽  
Vol 22 (1) ◽  
pp. 147032032199949
Author(s):  
Miaomiao Sang ◽  
Yu Fu ◽  
Chenmin Wei ◽  
Jing Yang ◽  
Xueting Qiu ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Primary Aldosteronism ◽  
Cardiovascular Events ◽  
Statistical Significance ◽  
Enzyme Linked Immunosorbent Assay ◽  
Microvascular Endothelial ◽  
Pai 1 ◽  
Microvascular Endothelial Function

Introduction: Studies have shown that primary aldosteronism (PA) has a higher risk of cardiovascular events than essential hypertension (EH). Endothelial dysfunction is an independent predictor of cardiovascular events. Whether PA and EH differ in the endothelial dysfunction is uncertain. Our study was designed to investigate the levels of biomarkers of endothelial dysfunction (Asymmetric dimethylarginine, ADMA; E-selectin, and Plasminogen activator inhibitor-1, PAI-1) and assess the microvascular endothelial function in patients with PA and EH, respectively. Methods: The biomarkers of endothelial dysfunction were measured by enzyme-linked immunosorbent assay (ELISA). Microvascular endothelial function was evaluated by Pulse amplitude tonometry (PAT). Results: Thirty-one subjects with EH and 36 subjects with PA including 22 with aldosterone-producing adenoma (APA) and 14 with idiopathic hyperaldosteronism (IHA) were enrolled in our study. The ADMA levels among the three groups were different (APA 47.83 (27.50, 87.74) ng/ml vs EH 25.08 (22.44, 39.79) ng/ml vs IHA 26.00 (22.23, 33.75) ng/ml; p = 0.04), however, when the APA group was compared with EH and IHA group, there was no statistical significance (47.83 (27.50, 87.74) ng/ml vs 25.08 (22.44, 39.79) ng/ml for EH, p = 0.11; 47.83 (27.50, 87.74) ng/ml vs IHA 26.00 (33.75) ng/ml, p = 0.07). The results of ADMA levels are presented as Median (p25, p75). Whereas, levels of PAI-1 and E-selectin, microvascular endothelial function were not significantly different between PA and EH subjects. Conclusions: Our study shows no significant differences between PA and EH in terms of biomarkers of endothelial dysfunction and microvascular endothelial function. The microvascular endothelial function of PA and EH patients is comparable.

scholarly journals Circulating biologic markers of endothelial dysfunction in cerebral small vessel disease: A review

2015 ◽  
Vol 36 (1) ◽  
pp. 72-94 ◽  
Author(s):  
Anna Poggesi ◽  
Marco Pasi ◽  
Francesca Pescini ◽  
Leonardo Pantoni ◽  
Domenico Inzitari
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Small Vessel Disease ◽  
Brain Magnetic Resonance Imaging ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Perivascular Spaces ◽  
Vessel Disease ◽  
Brain Changes

The term cerebral small vessel disease (SVD) refers to a group of pathologic processes with various etiologies that affect small arteries, arterioles, venules, and capillaries of the brain. Magnetic resonance imaging (MRI) correlates of SVD are lacunes, recent small subcortical infarcts, white-matter hyperintensities, enlarged perivascular spaces, microbleeds, and brain atrophy. Endothelial dysfunction is thought to have a role in the mechanisms leading to SVD-related brain changes, and the study of endothelial dysfunction has been proposed as an important step for a better comprehension of cerebral SVD. Among available methods to assess endothelial function in vivo, measurement of molecules of endothelial origin in peripheral blood is currently receiving selective attention. These molecules include products of endothelial cells that change when the endothelium is activated, as well as molecules that reflect endothelial damage and repair. This review examines the main molecular factors involved in both endothelial function and dysfunction, and the evidence linking endothelial dysfunction with cerebral SVD, and gives an overview of clinical studies that have investigated the possible association between endothelial circulating biomarkers and SVD-related brain changes.

Sign in / Sign up

Export Citation Format

Share Document