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Objectives: The aim of this study was to evaluate the acute and chronic effects of mesoglycan on the endothelial function and arterial elastic properties in patients with metabolic syndrome (MetS).
Background: MetS is defined by a clustering of vascular risk factors that demand both pharmacologic and non-pharmacologic interventions, including body weight reductions and physical activity. The correction of endothelial dysfunction and arterial wall distensibility associated with MetS have lately received increasing interest.
Methods: Thirty consecutive ambulatory patients affected by MetS were 2:1 randomized in a double-blind fashion to receive mesoglycan or placebo, respectively. In the first phase of the study, we evaluated the acute effects of a single i.m. administration of mesoglycan (60 mg) or placebo on vascular reactivity, as assessed by brachial flow-mediated dilation (FMD). Then, patients were chronically treated with mesoglycan per os (50 mg twice a day) or placebo for 90 days. At the end of this period, vascular reactivity and the arterial wall elastic properties were evaluated.
Results: In the mesoglycan group, FMD increased above baseline after acute administration, with a maximum increment of 52% after 2 h. FMD was also significantly greater than baseline after 90 days of chronic treatment. In the placebo group, FMD was unaffected by both acute and chronic mesoglycan administration. Moreover, after 90 days of mesoglycan treatment, a marked improvement in arterial distensibility and compliance was detected and arterial stiffness reduced significantly.
Conclusions: This small, preliminary study shows that mesoglycan exerts relevant effects on vascular physiology, both in an acute setting as well as after prolonged, three-month treatment, in patients affected by metabolic syndrome.
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http://dx.doi.org/10.1016/j.atherosclerosis.2015.10.007 | DOI Listing |
Colloids Surf B Biointerfaces
August 2025
Department of Orthopedics, Affiliated Hospital of Jiangxi University of Chinese Medicine, Nanchang, Jiangxi 330006, China. Electronic address:
Infected wounds remain a major clinical challenge due to bacterial invasion, which disrupts the natural healing cascade through excessive reactive oxygen species (ROS) generation, severe vascular damage, and persistent inflammation. Inspired by the catechol-rich adhesive domains of mussel foot proteins, we developed an extracellular matrix (ECM)-mimetic polyethylene glycol (PEG) hydrogel incorporating polydopamine (PDA)-functionalized zinc oxide nanoparticles (ZnONPs) for infected wound therapy. The amino acid-functionalized PEG hydrogel reproduces ECM-like properties to facilitate cell migration and efficient exudate management; however, its lack of intrinsic antimicrobial activity limits therapeutic efficacy.
View Article and Find Full Text PDFFuture Sci OA
December 2025
Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto, Japan.
Background: Smoking induces inflammation in the heart and intima layer of blood vessels by activating nuclear factor kappa B, which controls the transcription of immunoglobulin free light chain (FLC)-κ. FLC levels are indicative of higher mortality in the overall population and poorer prognoses in cardiovascular diseases. This study aimed to analyze the effect of smoking cessation (SC) on the levels of FLCs and markers of inflammation and heart failure.
View Article and Find Full Text PDFNitric Oxide
September 2025
Department of Physics, Wake Forest University, Winston-Salem, NC 27109, USA; Translational Science Center, Wake Forest University, Winston-Salem, NC 27109, USA. Electronic address:
We recently demonstrated a rapid reaction between labile ferric heme and nitric oxide (NO) in the presence of reduced glutathione (GSH) or other small thiols in a process called thiol-catalyzed reductive nitrosylation, yielding a novel signaling molecule, labile nitrosyl ferrous heme (NO-ferroheme), which we and others have shown can regulate vasodilation and platelet homeostasis. Red blood cells (RBCs) contain high concentrations of GSH, and NO can be generated in the RBC via nitrite reduction and/or RBC endothelial nitric oxide synthase (eNOS) so that NO-ferroheme could, in principle, be formed in the RBC. NO-ferroheme may also form in other cells and compartments, including in plasma, where another small and reactive thiol species, hydrogen sulfide (HS/HS), is also present and may catalyze NO-ferroheme formation akin to GSH.
View Article and Find Full Text PDFFree Radic Biol Med
September 2025
Department of Cellular and Integrative Physiology, University of Nebraska Medical Center. Electronic address:
Background: Excessive oxidative stress is well known to participate in the pathogenesis of hypertension. A major regulator of oxidative stress is the transcription factor Nuclear factor erythroid 2-related factor 2 (Nrf2). However, the role of Nrf2 in the pathogenesis of hypertension is not completely understood, especially at the endothelial cell level.
View Article and Find Full Text PDFCan J Cardiol
September 2025
Division of Cardiology, Hartford HealthCare Heart and Vascular Institute, Hartford, CT, USA. Electronic address:
Post-transplant rejection surveillance remains a cornerstone of heart transplant care. Although endomyocardial biopsy (EMB) has long been the gold standard for detecting rejection, its invasive nature, interobserver variability in histologic interpretation, and limitations in distinguishing between acute cellular rejection (ACR) and antibody-mediated rejection have prompted interest in noninvasive techniques. Traditional biomarkers- such as troponin, C-reactive protein, brain natriuretic peptide, and donor-specific antibodies- offer supplementary assessments of graft function but lack the specificity and sensitivity required to be standalone markers.
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