Atherosclerotic cardiovascular disease (ASCVD) is the deadliest disease in the world, with endothelial injury occurring throughout the course of the disease. Therefore, improvement in endothelial function is of essential importance in the prevention of ASCVD. Red yeast rice (RYR), a healthy traditional Chinese food, has a lipid modulation function and also plays a vital role in the improvement of endothelial reactivity and cardiovascular protection; thus, it is significant in the prevention and treatment of ASCVD. This article reviews the molecular mechanisms of RYR and its related products in the improvement of endothelial function in terms of endothelial reactivity, anti-apoptosis of endothelial progenitor cells, oxidative stress alleviation and anti-inflammation.
Apoptosis ; drug effects ; Atherosclerosis ; pathology ; physiopathology ; prevention & control ; Biological Products ; chemistry ; pharmacology ; therapeutic use ; Cardiovascular Diseases ; pathology ; physiopathology ; prevention & control ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; therapeutic use ; Endothelium, Vascular ; cytology ; drug effects ; physiology ; Humans ; Inflammation ; prevention & control ; Lipid Metabolism ; drug effects ; Oxidative Stress ; drug effects

The incidence and mortality rates of diabetes with cardiovascular complications are continually rising, and diabetic cardiovascular disease is becoming a major public health issue that threatens human health. Acute endothelial dysfunction and chronic cellular damage caused by diabetes are important risk factors for diabetic cardiovascular disease and related mortality. Adiponectin is an adipocyte-derived molecule with significant cytoprotective effects, including the protection against diabetes-induced vascular endothelial injury. Here we review the mechanisms of adiponectin protective effects on acute vascular endothelial dysfunction and chronic structural damage induced by diabetes.
Adiponectin ; physiology ; Cardiovascular Diseases ; complications ; Diabetes Mellitus ; pathology ; Endothelium, Vascular ; physiopathology ; Humans

BACKGROUND: Hypertension and atherosclerosis are bidirectionally related, while platelet count could serve as an indicator of endothelial repair. Therefore, high platelet counts could be associated with hypertension by indicating more intense endothelial repair activity. Furthermore, short stature has been shown to constitute a risk of atherosclerosis. Since inflammation-related single-nucleotide polymorphism (SNP (rs3782886)) is reportedly associated with myocardial infarction and short stature, rs3782886 could be associated with a high platelet count and thus more intense endothelial repair activity. METHODS: We conducted a cross-sectional study of 988 elderly Japanese who participated in a general health check-up. Short stature was defined as a height of at or under the 25th percentile of the study population, and high platelet count as the highest tertiles of the platelet levels. RESULTS: High platelet counts were found to be independently and positively associated with hypertension while rs3782886 was independently associated with high platelet levels and short stature. The classical cardiovascular risk factor-adjusted odds ratio (OR) and 95% confidence interval (CI) of high platelet count for hypertension was 1.34 (1.02, 1.77). With non-minor homo of the rs3782886 as the reference group, the adjusted OR and 95% CI for high platelet count and short stature of minor home were 2.40 (1.30, 4.42) and 2.21 (1.16, 4.21), respectively. CONCLUSION SNP (rs3782886) was shown to be associated with high platelet count and short stature. This result partly explains how a genetic factor can influence the impact of height on endothelial repair.
Aged ; Aged, 80 and over ; Blood Platelets ; metabolism ; Body Height ; genetics ; Cross-Sectional Studies ; Endothelium, Vascular ; physiology ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genotype ; Humans ; Hypertension ; blood ; epidemiology ; genetics ; Male ; Middle Aged ; Odds Ratio ; Platelet Count ; Polymorphism, Single Nucleotide

Apoptosis ; Endoplasmic Reticulum ; pathology ; Endothelium, Vascular ; pathology ; Gene Expression Regulation ; physiology ; Humans ; Stress, Physiological

PURPOSE: Endothelial dysfunction (ED) is a pivotal phenomenon in the development of cardiovascular disease (CVD) in patients receiving hemodialysis (HD). Indoxyl sulfate (IS) is a known uremic toxin that induces ED in patients with chronic kidney disease. The aim of this study was to investigate whether AST-120, an absorbent of IS, improves microvascular or macrovascular ED in HD patients. MATERIALS AND METHODS: We conducted a prospective, case-controlled trial. Fourteen patients each were enrolled in respective AST-120 and control groups. The subjects in the AST-120 group were treated with AST-120 (6 g/day) for 6 months. Microvascular function was assessed by laser Doppler flowmetry using iontophoresis of acetylcholine (Ach) and sodium nitroprusside (SNP) at baseline and again at 3 and 6 months. Carotid arterial intima-media thickness (cIMT) and flow-mediated vasodilation were measured at baseline and 6 months. The Wilcoxon rank test was used to compare values before and after AST-120 treatment. RESULTS: Ach-induced iontophoresis (endothelium-dependent response) was dramatically ameliorated at 3 months and 6 months in the AST-120 group. SNP-induced response showed delayed improvement only at 6 months in the AST-120 group. The IS level was decreased at 3 months in the AST-120 group, but remained stable thereafter. cIMT was significantly reduced after AST-120 treatment. No significant complications in patients taking AST-120 were reported. CONCLUSION: AST-120 ameliorated microvascular ED and cIMT in HD patients. A randomized study including a larger population will be required to establish a definitive role of AST-120 as a preventive medication for CVD in HD patients.
Acetylcholine ; Adult ; Carbon/*therapeutic use ; Cardiovascular Diseases/etiology/*prevention & control ; Carotid Intima-Media Thickness ; Endothelium, Vascular/*physiopathology ; Female ; Humans ; Iontophoresis ; Kidney Failure, Chronic/complications/*physiopathology/*therapy ; Laser-Doppler Flowmetry ; Male ; Microcirculation/physiology ; Middle Aged ; Nitroprusside ; Oxides/*therapeutic use ; Prospective Studies ; *Renal Dialysis ; Young Adult

In recent years, injuries induced by explosive blast have got more and more attention owing to weapon development and frequent terrorist activities. Tear, bleeding and edema of tissues and organs are the main manifestations of blast shock wave damage. Vascular endothelial barrier is the main defense of tissues and organs' integrity. This article aims to discuss possible mechanisms of endothelial barrier damage induced by explosive blast and main manifestations of blood brain barrier, bloodeair barrier, and intestinal vascular barrier impairments. In addition, the main regulatory factors of vascular permeability are also summarized so as to provide theoretical basis for prevention and cure of vascular endothelial barrier damage resulting from explosive blast.
Blast Injuries ; metabolism ; Blood-Brain Barrier ; Capillary Permeability ; Endothelium, Vascular ; metabolism ; Humans ; Nitric Oxide ; physiology ; Platelet Activating Factor ; physiology ; Serotonin ; physiology ; Thrombin ; physiology

OBJECTIVEThis study aimed to evaluate the vascular endothelial growth factor (VEGF) expression and permeability of vascular endothelial cell under microvibration.

METHODSHuman umbilical vein endothelial cell (HUVEC) were cultured, randomly vibrated under low frequency of 0.2, 0.5, 2, 5 Hz, 30 min per day. The VEGF mRNA level was detected by Tagman probe real-time fluorescence quantitative polymerase chain reaction (PCR), and the VEGF protein expression level was detected by Western blot. The permeability of vascular endothelial cell was evaluated.

RESULTSCompared with the blank control group, the mRNA and protein expression level of VEGF were significantly increased under 0.2, 0.5 Hz thelial, and increase the permeability microvibration (P<0.05), and decreased under 2, 5 Hz microvibration (P<0.01). The vascular endothelial permeability in creased under 0.2, 0.5 Hz microvibration (P<0.01), whereas the permeability decreased under 2, 5 Hz microvibration (P<0.01).

CONCLUSION0.2-0.5 Hz microvibration can up-regulate the expression of VEGF mRNA and protein in vascular endothelial, and increase the permeability.

Blotting, Western ; Capillary Permeability ; physiology ; Endothelial Cells ; metabolism ; Endothelium, Vascular ; chemistry ; Humans ; Permeability ; Polymerase Chain Reaction ; RNA, Messenger ; analysis ; Umbilical Cord ; chemistry ; metabolism ; Up-Regulation ; Vascular Endothelial Growth Factor A ; analysis ; genetics ; physiology

OBJECTIVETo study the effect of gastrodin on isolated thoracic aorta rings of rats and to investigate the potential mechanism.

METHODSA perfusion model of isolated thoracic aorta rings of rats was applied. The effect of cumulative gastrodin (5, 50, 100,150, 200, and 250 μmol/L) on endothelium-intact aorta rings was investigated. The same procedure was applied to observe the effect of gastrodin on endothelium-intact/denuded aorta rings pre-contracted with 10(-6) mol/L phenylephrine hydrochloride (PE). The aorta rings incubated by 200 mmol/L gastrodin in the Ca(2+)-free (K-H) solution was contracted by using PE. The effect of 200 mmol/L gastrodin on endothelium-denuded aorta rings pre-contracted with 60 mmol/L KCl was also observed.

RESULTSCompared with the denuded gastrodin group, the intact gastrodin group could significantly relax the PE-contracted aorta rings (P<0.01). In Ca(2+)-free (K-H) solution KHS, the PE-induced contraction rate of aorta rings pre-incubated by gastrodin was 6.5%±0.7%, which was significantly less than the control group (11.8%±0.9%,P<0.01). However, after 3 mmol/L CaCl2 was added, the Ca(2+)-induced contraction in the gastrodin group (51.7%±2.4%) was similar to that in the control group (49.8%±2.8%). The contractile rate of rings in the KCl-contracted gastrodin group (96.3%±0.6%) was not significantly different from that in the control group (96.8%±1.2%).

CONCLUSIONSGastrodin has the effect of vasorelaxation on isolated thoracic aorta rings of rats. The mechanism of the vasorelaxation of gastrodin may mainly work through the inhibition of inositol 1, 4, 5-trisphosphosphate receptor on the sarcoplasmic reticulum of the arterial smooth muscle, which leads to the reduction of the Ca(2+) released from the sarcoplasmic reticulum.

Animals ; Aorta, Thoracic ; drug effects ; physiology ; Benzyl Alcohols ; pharmacology ; Calcium ; metabolism ; Endothelium, Vascular ; physiology ; Female ; Glucosides ; pharmacology ; In Vitro Techniques ; Male ; Phenylephrine ; pharmacology ; Rats ; Rats, Wistar ; Vasodilation ; drug effects

The vascular endothelium is a dynamic structure responsible for the separation and regulated movement of biological material between circulation and interstitial fluid. Hormones and nutrients can move across the endothelium either via a transcellular or paracellular route. Transcellular endothelial transport is well understood and broadly acknowledged to play an important role in the normal and abnormal physiology of endothelial function. However, less is known about the role of the paracellular route. Although the concept of endothelial dysfunction in diabetes is now widely accepted, we suggest that alterations in paracellular transport should be studied in greater detail and incorporated into this model. In this review we provide an overview of endothelial paracellular permeability and discuss its potential importance in contributing to the development of diabetes and associated complications. Accordingly, we also contend that if better understood, altered endothelial paracellular permeability could be considered as a potential therapeutic target for diabetes.
Adherens Junctions ; Adiponectin ; Endothelium ; Endothelium, Vascular ; Extracellular Fluid ; Insulin ; Permeability ; Physiology ; Tight Junctions

OBJECTIVETo investigate the effects of microvesicles (MVs) derived from hypoxia/reoxygenation (H/R)-treated human umbilical vein endothelial cells (HUVECs) on endothelium-dependent relaxation of rat thoracic aortic rings.

METHODSH/R injury model was established to induce HUVECs to release H/R-EMVs. H/R-EMVs from HUVECs were isolated by ultracentrifugation from the conditioned culture medium. H/R-EMVs were characterized using 1 μm latex beads and anti-PE-CD144 by flow cytometry. Thoracic aortic rings of rats were incubated with 2.5, 5, 10, 20 μg/ml H/R-EMVs derived from H/R-treated HUVECs for 4 hours, and their endothelium-dependent relaxation in response to acetylcholine (ACh) or endothelium-independent relaxation in response to sodium nitroprusside (SNP) was recorded in vitro. The nitric oxide (NO) production of ACh-treated thoracic aortic rings of rats was measured using Griess reagent. The expression of endothelial NO synthase (eNOS) and phosphorylated eNOS (p-eNOS, Ser-1177) in the thoracic aortic rings of rats was detected by Western blotting. Furthermore, the levels of SOD and MDA in H/R-EMVs-treated thoracic aortic rings of rats were measured using SOD and MDA kit.

RESULTSH/R-EMVs were induced by H/R-treated HUVECs and isolated by ultracentrifugation. The membrane vesicles (< 1 μm) induced by H/R were CD144 positive. ACh-induced relaxation and NO production of rat thoracic aortic rings were impaired by H/R-EMVs treatment in a concentration-dependent manner (P < 0.05, P < 0.01). The expression of total eNOS (t-eNOS) was not affected by H/R-EMVs. However, the expression of p-eNOS decreased after treated with H/R-EMVs. The activity of SOD decreased and the level of MDA increased in H/R-EMVs treated rat thoracic aortic rings (P < 0.01).

CONCLUSIONACh induced endothelium-dependent relaxation of thoracic aortic rings of rats was impaired by H/R-EMVs in a concentration-dependent manner. The mechanisms included a decrease in NO production, p-eNOS expression and an increase in oxidative stress.

Acetylcholine ; pharmacology ; Animals ; Aorta, Thoracic ; physiology ; Cell Hypoxia ; Endothelium, Vascular ; physiology ; Human Umbilical Vein Endothelial Cells ; cytology ; Humans ; In Vitro Techniques ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase Type III ; metabolism ; Nitroprusside ; pharmacology ; Oxidative Stress ; Rats