Even though an association between inflammation and hypertension has been known for many years, it has not been simple to ascertain the role of several physiological responses involved. The innate immune response plays a critical role in these physiological responses. Innate immune cells can be activated directly by shear stress, activate the inflammasome and produce numerous cytokines and soluble mediators essential in hypertension. NFkB activation is mainly involved in the activation of innate immune cells. Shear stress also stimulates the expression of DAMP and PAMP receptors, enhancing pathogen and danger signals and magnifying inflammation. The adaptative immune response is activated with the increased antigen presentation resulting from the insults mentioned. Chronic inflammation may lead to autoimmunity. Peripheral hypoxia, a consequence of hypertension, activates hypoxia-inducing factors 1-α and 1-β (HIF-1α, HIF-1β), which modulate innate immune cells and promote inflammation. HIF-1α is involved in the upregulation of oxygen and nitrogen radical production proteins. HIF-1β down-regulates antioxidant enzymes. However, the critical evidence of the role of innate immune cells in hypertension came from the results of clinical trials involving therapies blocking inflammatory cytokines and Toll-like receptor expression. Several lines of research have been conducted on this complex disease. Pro-tolerogenic innate immune cells, myeloid suppressor cells, and M2 macrophages may play a crucial role in promoting or resolving inflammation, cardiovascular diseases and hypertension, and should be studied in detail.

• MeSH
• cytokiny metabolismus   MeSH
• hypertenze * MeSH
• hypoxie MeSH
• lidé MeSH
• přirozená imunita * MeSH
• zánět metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

BACKGROUND: Morbidity and mortality from COVID-19 caused by novel coronavirus SARS-CoV-2 is accelerating worldwide, and novel clinical presentations of COVID-19 are often reported. The range of human cells and tissues targeted by SARS-CoV-2, its potential receptors and associated regulating factors are still largely unknown. The aim of our study was to analyze the expression of known and potential SARS-CoV-2 receptors and related molecules in the extensive collection of primary human cells and tissues from healthy subjects of different age and from patients with risk factors and known comorbidities of COVID-19. METHODS: We performed RNA sequencing and explored available RNA-Seq databases to study gene expression and co-expression of ACE2, CD147 (BSG), and CD26 (DPP4) and their direct and indirect molecular partners in primary human bronchial epithelial cells, bronchial and skin biopsies, bronchoalveolar lavage fluid, whole blood, peripheral blood mononuclear cells (PBMCs), monocytes, neutrophils, DCs, NK cells, ILC1, ILC2, ILC3, CD4+ and CD8+ T cells, B cells, and plasmablasts. We analyzed the material from healthy children and adults, and from adults in relation to their disease or COVID-19 risk factor status. RESULTS: ACE2 and TMPRSS2 were coexpressed at the epithelial sites of the lung and skin, whereas CD147 (BSG), cyclophilins (PPIA andPPIB), CD26 (DPP4), and related molecules were expressed in both epithelium and in immune cells. We also observed a distinct age-related expression profile of these genes in the PBMCs and T cells from healthy children and adults. Asthma, COPD, hypertension, smoking, obesity, and male gender status generally led to the higher expression of ACE2- and CD147-related genes in the bronchial biopsy, BAL, or blood. Additionally, CD147-related genes correlated positively with age and BMI. Interestingly, we also observed higher expression of CD147-related genes in the lesional skin of patients with atopic dermatitis. CONCLUSIONS: Our data suggest different receptor repertoire potentially involved in the SARS-CoV-2 infection at the epithelial barriers and in the immune cells. Altered expression of these receptors related to age, gender, obesity and smoking, as well as with the disease status, might contribute to COVID-19 morbidity and severity patterns.

• MeSH
• angiotensin konvertující enzym 2 genetika   imunologie   MeSH
• basigin genetika   imunologie   MeSH
• bronchiální astma epidemiologie   genetika   imunologie   MeSH
• chronická nemoc epidemiologie   MeSH
• chronická obstrukční plicní nemoc epidemiologie   genetika   imunologie   MeSH
• COVID-19 epidemiologie   genetika   imunologie   MeSH
• dipeptidylpeptidasa 4 genetika   imunologie   MeSH
• dítě MeSH
• dospělí MeSH
• exprese genu genetika   MeSH
• hypertenze epidemiologie   genetika   imunologie   MeSH
• kojenec MeSH
• komorbidita MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladiství MeSH
• mladý dospělý MeSH
• obezita epidemiologie   genetika   imunologie   MeSH
• předškolní dítě MeSH
• přirozená imunita imunologie   MeSH
• rizikové faktory MeSH
• SARS-CoV-2 genetika   imunologie   MeSH
• senioři MeSH
• věkové faktory MeSH
• Check Tag
• dítě MeSH
• dospělí MeSH
• kojenec MeSH
• lidé středního věku MeSH
• lidé MeSH
• mladiství MeSH
• mladý dospělý MeSH
• mužské pohlaví MeSH
• předškolní dítě MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

Metabolický syndróm sa definuje ako nenáhodný spoločný výskyt prediabetických stavov súvisiacich s inzulínovou rezistenciou, ako je hraničná glykémia nalačno, porušená glukózová tolerancia alebo hranične zvýšený glykovaný hemoglobín HbA1c, ďalej výskyt centrálnej obezity, aterogénnej dyslipidémie spojenej so zvýšením hladiny triacylglycerolov a znížením HDL-lipoproteínov s vyššou denzitou, artériovej hypertenzie a ďalších faktorov, ktoré sa podieľajú na zvýšenom riziku diabetes mellitus 2. typu a kardiovaskulárnych ochorení. V etiopatogenéze metabolického syndrómu sa uplatňuje expanzia dysfunkčného tukového tkaniva s aktiváciou imunitného systému, navodením subklinickej zápalovej reakcie a indukciou inzulínovej rezistencie zápalovými cytokínmi a lipidmi. Etiopatogenetické mechanizmy metabolického syndrómu, majú primárne adaptačný význam pri akútnej obrannej reakcii proti mikroorganizmom. Zápalom navodená inzulínová rezistencia v metabolických tkanivách je potrebná na presun glukózy k rýchlo proliferujúcim imunitným bunkám, využívajúcim aerobnú glykolýzu ako hlavný energetický mechanizmus. Cytokínmi indukovaná dyslipidémia (tzv. lipémia pri sepse) má protektívny význam pred poškodzujúcim účinkom endotoxínu. Hypertenzný, nátriumretenčný fenotyp zodpovedá za retenciu vody potrebnej pre metabolizmus proliferujúcich imunitných buniek a kompenzáciu strát tekutín napr. potením, vracaním a hnačkami pri infekciách. Pri ich dlhodobom pôsobení dôsledkom expanzie tukového tkaniva pri obezite vedú k vzniku metabolického syndrómu, diabetes mellitus 2. typu a kardiovaskulárnych ochorení.

Metabolic syndrome is defined as cluster of independent risk factors of type 2 diabetes mellitus and cardiovascular diseases including prediabetic states associated with insulin resistance as impaired fasting glucose, impaired glucose tolerance and/or bordering increased glycosylated haemoglobin; central obesity, atherogenic dyslipidaemia with increasing of triglyceride levels and decreasing of high density lipoprotein levels and hypertension. Etiopathogenesis of metabolic syndrome implements expansion of dysfunctional adipose tissue with activation of immune system, induction of low grade inflammatory reaction and induction of insulin resistance by cytokine and lipids. Etiopathogenetic mechanisms of metabolic syndrome have primary adaptive importance in acute defence reaction against microorganism. Inflammatory induced insulin resistance in metabolic tissues is necessary for relocation of glucose to rapid proliferated immune cells utilised aerobic glycolysis such main energetic mechanism. Cytokines induced dyslipidaemia (lipaemia of sepsis) has protective value against destructive effect of endotoxin. Hypertensive sodium retention phenotype is responsible for water retention required for metabolism of proliferative immune cells and compensation of fluid losses by e.g. perspiration, vomiting and diarrhoea during infections. Their long-acting effect due to expansion of adipose tissue in obesity is associated with metabolic syndrome, type 2 diabetes mellitus and cardiovascular diseases.

• MeSH
• dyslipidemie MeSH
• inzulinová rezistence MeSH
• lidé MeSH
• metabolický syndrom * patofyziologie   MeSH
• zánět MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy MeSH

Adipose tissue (AT) lies at the crossroad of nutrition, metabolism, and immunity; AT inflammation was proposed as a central mechanism connecting obesity with its metabolic and vascular complications. Resident immune cells constitute the second largest AT cellular component after adipocytes and as such play important roles in the maintenance of AT homeostasis. Obesity-induced changes in their number and activity result in the activation of local and later systemic inflammatory response, marking the transition from simple adiposity to diseases such as type 2 diabetes mellitus, arterial hypertension, and ischemic heart disease. This review has focused on the various subsets of immune cells in AT and their role in the development of AT inflammation and obesity-induced insulin resistance.

• MeSH
• inzulinová rezistence imunologie   MeSH
• lidé MeSH
• lymfocyty imunologie   patologie   MeSH
• myeloidní buňky imunologie   patologie   MeSH
• obezita etiologie   imunologie   patologie   MeSH
• tuková tkáň imunologie   metabolismus   patologie   MeSH
• zánět etiologie   imunologie   patologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

OBJECTIVE: To investigate the effect of long-term catecholamine excess in pheochromocytoma on leukocyte and platelet count and on proteins of acute-phase response. METHODS: Fifteen subjects with pheochromocytoma, 16 with primary aldosteronism, 18 with essential hypertension and 17 healthy controls were studied. Sixteen subjects with pheochromocytoma were investigated after tumor removal. Leukocyte, neutrophil and platelet count, as well as C-reactive protein were measured in all subjects, while fibrinogen, alpha(1)-antitrypsin, alpha(2)-macroglobulin, orosomucoid, transferrin and prealbumin were only measured in subjects with pheochromocytoma, primary aldosteronism and essential hypertension. RESULTS: Subjects with pheochromocytoma showed significantly higher leukocyte [7.5 +/- 0.9 10(9)/l, p < 0.001 vs. primary aldosteronism (5.4 +/- 0.9 10(9)/l) and healthy controls (5 +/- 0.9 10(9)/l), p = 0.04 vs. essential hypertension (6.3 +/- 1.6 10(9)/l)], neutrophil (p < 0.001 vs. primary aldosteronism and healthy subjects) and platelet counts (p < 0.001 vs. primary aldosteronism; p = 0.01 vs. essential hypertension) compared to the other groups of subjects. Similar results were obtained for positive proteins of acute-phase response in subjects with pheochromocytoma [C-reactive protein: 0.62 +/- 0.52 mg/dl, p < 0.001 vs. healthy subjects (0.08 +/- 0.08 mg/dl), p = 0.001 vs. primary aldosteronism (0.17 +/- 0.19 mg/dl), p = 0.04 vs. essential hypertension (0.31 +/- 0.26 mg/dl); fibrinogen: p = 0.02 vs. primary aldosteronism; orosomucoid: p = 0.005 vs. primary aldosteronism; alpha(2)-macroglobulin: p = 0.009 vs. primary aldosteronism]. No significant differences were found in plasma levels of alpha(1)-antitrypsin, transferrin and prealbumin. Tumor removal led to a significant decrease in leukocyte (p = 0.004), neutrophil (p = 0.007) and platelet count (p = 0.003) and also to a significant decrease in acute-phase proteins (C-reactive protein: p = 0.03, fibrinogen: p = 0.008, alpha(1)-antitrypsin: p = 0.003, orosomucoid: p = 0.04). CONCLUSIONS: Chronic catecholamine excess in pheochromocytoma is accompanied by an increase in inflammation markers which was reversed by the tumor removal. Copyright 2007 S. Karger AG, Basel.

• MeSH
• alfa-1-antitrypsin krev   MeSH
• alfa-makroglobuliny analýza   MeSH
• biologické markery krev   MeSH
• C-reaktivní protein analýza   MeSH
• dospělí MeSH
• feochromocytom komplikace   krev   patofyziologie   MeSH
• fibrinogen analýza   MeSH
• financování organizované MeSH
• hyperaldosteronismus komplikace   krev   patofyziologie   MeSH
• hypertenze etiologie   krev   MeSH
• lidé středního věku MeSH
• lidé MeSH
• nádory nadledvin komplikace   krev   patofyziologie   MeSH
• neutrofily MeSH
• orosomukoid analýza   MeSH
• počet leukocytů MeSH
• počet trombocytů MeSH
• prealbumin analýza   MeSH
• transferin analýza   MeSH
• zánět komplikace   krev   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH

V patogenezi aterosklerózy jsou kromě tradič ních rizikových faktorů , jako je hypertenze, hyperlipoproteinémie, diabetes mellitus, obezita a kouření, v posledních 20 letech diskutovány i další faktory, mezi které patří infekce a chronický zánět. Pů vodní koncepci možné úlohy speci- fického infekního agens, např. Chlamydia pneumoniae, cytomegalovirus či Helicobacter pylori vystřídala teorie synergického působení více patogenů, přičemž každý z nich může přispívat k pomalému chronickému zánětu. Předčasná manifestace aterosklerózy byla popsána i u tzv. autoimunitních onemocnění. Jedná se především o systémový lupus erythematodes (SLE), revmatoidní artritidu (RA) a antifosfolipidový syn-drom (APS). Ateroskleróza je chronické fibroproliferativní onemocnění, které je iniciované poškozením endotelu a které je řízeno mechanismy vrozené i získané imunity. Z inflamatorních markerů je ke stanovení míry kardiovaskulárního rizika stále nejčastěji používán ultrasenzitivně měřený CRP. Ostatní parametry jsou zatím využívány spíše v experimentu. V terapii aterosklerózy se kromě kyseliny acetylsalicylové připisují antiinflamatorní vlastnosti i lékům, jako jsou statiny, ACE inhibitory či sartany. Výrazný efekt by mohla přinést biologická léčba.

Besides traditional cardiovascular risk factors, e.g. hypertension, hyperlipoproteinemia, diabetes mellitus, obesity or smoking , there are new factors being discussed, such as infection and chronic inflammation, which may play a crucial role in the pathogenesis of ather osclerosis. The first conception of one single infectious agent, e.g Chlamydia pneumoniae , cytomegalovirus or Helicobacter pylori has been replaced by the theory of a synergistic effect of multiple pathogens; each of them may contribute to chronic low-grade inflammation. Premature atherosclerosis manifestation has been further observed in patients with autoimmune diseases: systemic lupus erythematodes (SLE), rheumatoid ar thritis (RA) or antiphospholipid syndrome (APS). Atherosclerosis is a chronic fibroproliferative disease initiated by endothelial damage, wh ich is regulated by mechanisms of both innate and adaptive immunity. Among inflammatory markers, ultrasensitive measurement of CRP is the most c ommonly used for cardiovascular risk assessment. Other parameters are used mostly in experiment. Besides acetylsalicylic acid, certain anti-inflammatory properties have been attributed to other drugs commonly used in patients with advanced atherosclerosis: statins, ACE inhibitors , angiotensin receptor blockers. Experiments with biologic therapy are promising.

• MeSH
• adaptivní imunita MeSH
• adiponektin MeSH
• alergologie a imunologie MeSH
• aterosklerotický plát * klasifikace   patofyziologie   MeSH
• ateroskleróza * etiologie   patofyziologie   MeSH
• autoimunitní nemoci MeSH
• biologické markery * MeSH
• C-reaktivní protein diagnostické užití   MeSH
• Chlamydophila pneumoniae patogenita   MeSH
• cytomegalovirové infekce MeSH
• diagnostické techniky a postupy MeSH
• fibrinogen MeSH
• Helicobacter pylori MeSH
• imunitní systém MeSH
• inhibitor aktivátoru plazminogenu 1 MeSH
• interleukin-18 MeSH
• klinické zkoušky jako téma MeSH
• lidé MeSH
• makrofágy MeSH
• monocyty MeSH
• Porphyromonas gingivalis patogenita   MeSH
• přirozená imunita MeSH
• prospektivní studie MeSH
• rizikové faktory MeSH
• T-lymfocyty MeSH
• zánět * MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy MeSH

ÚVOD: Akútny kompartment syndróm vzniká náhlym zvýšením tlaku v anatomickom priestore, ktorý je ohraničený málo poddajným obalom. Zmnoženie obsahu brušnej dutiny pri nízkej elasticite ohraničujúcich štruktúr spôsobuje intraabdominálnu hypertenziu s poklesom perfúzneho tlaku. METODIKA A VÝSLEDKY: Hypoperfúzia s ischémiou čreva a ďalších intraperitoneálnych a retroperitoneálnych štruktúr vedie k poruche metabolizmu s nedostatočnou tvorbou energie, tvorbou voľných kyslíkových radikálov a produkciou cytokínov, ktoré iniciujú rozvoj zápalovej reakcie. Ischemická, edematózna črevná stena stráca funkciu bariéry, translokácia endotoxínov a fekálnych baktérií do lymfatického systému vedie ku generalizácii zápalovej reakcie. V štádiu reperfúzie sa ischémiou poškodené tkanivá stávajú zdrojom prozápalových mediátorov, ampli!kujúcich systémovú zápalovú reakciu. Zvýšený intraabdominálny tlak ovplyvňuje nielen funkciu orgánov a tkanív brušnej dutiny (solídne orgány - pečeň, slezina, duté orgány - žalúdok, črevo a cievy), ale prenáša sa aj na ďalšie telové kompartmenty. Charakteristické sú hemodynamické zmeny, poruchy respirácie, akútna renálna insu!ciencia a ďalšie. Ovplyvnenie sa realizuje mechanicky (vysoký stav bránice), humorálne (cievny systém, imunitný systém, endokrínny systém) a prostredníctvom nervového systému. ZÁVER: Akútny abdominálny kompartment syndróm je veľmi závažnou komplikáciou kriticky chorých pacientov nielen pre jeho intraabdominálny efekt, ale aj pre ovplyvnenie funkcie vzdialených systémov. Nie je samostatným ochorením, ale syndrómom, tvoreným symptómami, ktoré môžu mať rôzne príčiny. Ak sa včas nediagnostikuje a nelieči vedie k multiorgánovému zlyhávaniu (MODS – multiple organ dysfunction syndrome), zlyhaniu (MOFS - multiple organ failure syndrome), prípadne až k smrti.

INTRODUCTION: Acute compartment syndrome is caused by rapid pressure increase within an anatomically de!ned space encased by considerably a more ore less non-elastic mantle. Augmentation of the inner content of abdominal cavity wrapped by structures with low elasticity leads to an intra-abdominal hypertension accompanied by decrease in perfusion pressure. METHODS, RESULTS: Hypoperfusion and ischemia of the bowels and other intra/retroperitoneal structures causes a metabolic malfunction associated with low energy production, free oxygen radicals and release of cytokines initiating the development of an in"ammatory reaction. Ischemic and oedematous wall of the intestine looses its barrier function, which in turn leads to a translocation of endotoxines and fecal bacteria into the lymphatic system, followed by generalized in"ammatory reaction. In the reperfusion phase, ischemically damaged tissues become a source of proin"ammatory mediators, amplifying the systemic in"ammatory reaction. Increased intra-abdominal pressure in"uences the functioning of organs and tissues of the abdominal cavity (solid organs – liver, spleen; hollow organs – stomach, intestine and vessels) and transmits its e#ects on other body compartments, as well. Typical changes being observed are hemodynamic and respiratory disorders, acute renal insu $ciency etc. These are mediated by mechanical (high position of the diaphragm), humoral (vascular, immune, endocrine system) and nervesystem associated pathways. CONCLUSIONS: Acute abdominal compartment syndrome is a serious complication in critically ill patients because of both direct intra-abdominal e#ect and also its impact on remote body systems. It is not considered as an isolated illness, but rather as a syndrome created by symptoms of various origins. If not diagnosed/treated early, it leads to MODS (multiple organ dysfunction syndrome), MOFS (multiple organ failure syndrome) or even to a death.

• MeSH
• acidóza etiologie   patofyziologie   MeSH
• biologické markery * MeSH
• C-reaktivní protein MeSH
• cytokiny fyziologie   krev   MeSH
• hypovolemie etiologie   patofyziologie   MeSH
• játra krevní zásobení   metabolismus   MeSH
• ledviny metabolismus   MeSH
• lidé MeSH
• multiorgánové selhání etiologie   MeSH
• nitrobřišní hypertenze * diagnóza   etiologie   patofyziologie   MeSH
• péče o pacienty v kritickém stavu MeSH
• renální insuficience etiologie   patofyziologie   MeSH
• respirační acidóza etiologie   patofyziologie   MeSH
• splanchnický oběh MeSH
• tlak škodlivé účinky   MeSH
• zánět etiologie   patofyziologie   MeSH
• Check Tag
• lidé MeSH

• MeSH
• angina pectoris farmakoterapie   patologie   MeSH
• antihypertenziva farmakologie   terapeutické užití   MeSH
• arterioskleróza patologie   MeSH
• biologické markery MeSH
• farmakoterapie metody   MeSH
• hodnocení léčiv MeSH
• lidé MeSH
• zánět patologie   MeSH
• Check Tag
• lidé MeSH

Hypercholesterolemia is one of primary risk factors of cardiovascular disease, together with metabolic syndrome, hypertension and diabetes. Although progress has been made, the search for novel methods of preventing and treating dyslipidemia is ongoing and current therapies for cardiovascular disease induce various side effects. β‑glucans are linear unbranched polysaccharides found in various natural sources, such as mushrooms. Due to their structure they are able to interact with innate immunity receptors, however they also act as dietary fibers in the digestive tract. As there are two forms of β‑glucans, insoluble and soluble forms, they are able to interact with lipids and biliary salts in the bowel and consequently reduce cholesterol levels. Therefore, they may be developed as a suitable therapeutic option to treat patients with dyslipidemia, as they are natural molecules that do not induce any significant side effects. The current review discusses the evidence supporting the effects of β‑glucans on cholesterol levels.

• MeSH
• anticholesteremika chemie   terapeutické užití   MeSH
• beta-glukany chemie   terapeutické užití   MeSH
• cholesterol krev   imunologie   metabolismus   MeSH
• hypercholesterolemie krev   imunologie   metabolismus   terapie   MeSH
• imunologické faktory chemie   terapeutické užití   MeSH
• lidé MeSH
• potravní vláknina analýza   terapeutické užití   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

BACKGROUND: C-reactive protein (CRP) is an acute inflammatory protein detected in obese patients with metabolic syndrome. Moreover, increased CRP levels have been linked with atherosclerotic disease, congestive heart failure, and ischemic heart disease, suggesting that it is not only a biomarker but also plays an active role in the pathophysiology of cardiovascular diseases. Since endothelial dysfunction plays an essential role in various cardiovascular pathologies and is characterized by increased expression of cell adhesion molecules and inflammatory markers, we aimed to detect specific markers of endothelial dysfunction, inflammation, and oxidative stress in spontaneously hypertensive rats (SHR) expressing human CRP. This model is genetically predisposed to the development of the metabolic syndrome. METHODS: Transgenic SHR male rats (SHR-CRP) and non-transgenic SHR (SHR) at the age of 8 months were used. Metabolic profile (including serum and tissue triglyceride (TAG), serum insulin concentrations, insulin-stimulated incorporation of glucose, and serum non-esterified fatty acids (NEFA) levels) was measured. In addition, human serum CRP, MCP-1 (monocyte chemoattractant protein-1), and adiponectin were evaluated by means of ELISA, histological analysis was used to study morphological changes in the aorta, and western blot analysis of aortic tissue was performed to detect expression of endothelial, inflammatory, and oxidative stress markers. RESULTS: The presence of human CRP was associated with significantly decreased insulin-stimulated glycogenesis in skeletal muscle, increased muscle and hepatic accumulation of TAG and decreased plasmatic cGMP concentrations, reduced adiponectin levels, and increased monocyte chemoattractant protein-1 (MCP-1) levels in the blood, suggesting pro-inflammatory and presence of multiple features of metabolic syndrome in SHR-CRP animals. Histological analysis of aortic sections did not reveal any visible morphological changes in animals from both SHR and SHR-CRP rats. Western blot analysis of the expression of proteins related to the proper function of endothelium demonstrated significant differences in the expression of p-eNOS/eNOS in the aorta, although endoglin (ENG) protein expression remained unaffected. In addition, the presence of human CRP in SHR in this study did not affect the expression of inflammatory markers, namely p-NFkB, P-selectin, and COX2 in the aorta. On the other hand, biomarkers related to oxidative stress, such as HO-1 and SOD3, were significantly changed, indicating the induction of oxidative stress. CONCLUSIONS: Our findings demonstrate that CRP alone cannot fully induce the expression of endothelial dysfunction biomarkers, suggesting other risk factors of cardiovascular disorders are necessary to be involved to induce endothelial dysfunction with CRP.

• MeSH
• adiponektin MeSH
• aorta MeSH
• biologické markery metabolismus   MeSH
• C-reaktivní protein metabolismus   MeSH
• chemokin CCL2 MeSH
• hypertenze * MeSH
• inzuliny * metabolismus   MeSH
• krysa rodu rattus MeSH
• lidé MeSH
• metabolický syndrom * diagnóza   genetika   MeSH
• oxidační stres MeSH
• potkani inbrední SHR MeSH
• zánět MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• lidé MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH