The aim of the research is to study the effect of L-arginine, the precursor of nitric oxide, and aminoguanidine, the inhibitor of inducible nitric oxide synthase, on morpho-functional changes in the liver of BALB/c mice with antiphospholipid syndrome. The study was carried out on 50 female BALB/c mice modelled with antiphospholipid syndrome. L-arginine (25 mg/kg) and aminoguanidine (10 mg/kg) were used for its correction. The material for microscopic study was taken by the method of Horalsky. The liver tissue samples were stained with hematoxylin and eosin. Significant hemodynamic disorders with manifestations of thrombosis in the liver in cases of antiphospholipid syndrome followed by destructive-degenerative changes of the stoma and parenchyma have been established. Administration of L-arginine in antiphospholipid syndrome caused restoration of the lobular and beam organization of the liver. The maximum effect on the morphological state of the liver was observed in using a combination of L-arginine and aminoguanidine. The protective effect of L-arginine and aminoguanidine on the microcirculation has been proved that evidences liver function restoration in mice with antiphospholipid syndrome.
Download full-text PDF |
Source |
---|
Cureus
December 2024
Neurology and Neuroscience, Medical University of Varna, Varna, BGR.
Neuromyelitis optica spectrum disorder (NMOSD) includes conditions with autoimmune genesis, which are manifested by attacks of optic neuritis (ON) and transverse myelitis (TM), and also express aquaporin 4 (NMO-IgG) or myelin oligo-endocytic glycoprotein (MOGAb) antibodies. In rare cases, the disease may also have a clinical presentation with only TM, without ON or with ON, without TM. These conditions are also included in the spectrum.
View Article and Find Full Text PDFCirc J
January 2025
Department of Radioisotope Medicine, Atomic Bomb Disease and Hibakusha Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University.
Antiphospholipid syndrome is an autoimmune disease characterised by thrombotic and/or obstetric manifestations with persistent antiphospholipid antibodies. Diagnosis involves confirming the persistence of antiphospholipid antibodies in symptomatic patients, using validated classification criteria as a guide. The likelihood of obtaining false-positive or false-negative test results in certain settings, and the lack of standardisation between laboratory methods, are important considerations.
View Article and Find Full Text PDFThromb Haemost
January 2025
Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Thrombocytopenia is one of the most common manifestations of the antiphospholipid syndrome (APS). However, its causes are still poorly defined. We have shown recently that antiphospholipid antibodies (aPL) directed against β2-glycoprotein I (β2GPI) of the IgG isotype induced platelet activation and aggregation while aPL directed against cardiolipin and anti-β2GPI IgM had no effect.
View Article and Find Full Text PDFMolecules
December 2024
Laboratory of Hemostasis, Hemocentro-Unicamp, Universidade Estadual de Campinas, Campinas 13083-878, SP, Brazil.
Machine learning and artificial intelligence tools were used to investigate the discriminatory potential of blood serum metabolites for thromboembolism and antiphospholipid syndrome (APS). H-NMR-based metabonomics data of the serum samples of patients with arterial or venous thromboembolism (VTE) without APS (n = 32), thrombotic primary APS patients (APS, n = 32), and healthy controls (HCs) (n = 32) were investigated. Unique metabolic profiles between VTE and HCs, APS and HCs, and between VTE and triple-positive APS groups were indicative of the significant alterations in the metabolic pathways of glycolysis, the TCA cycle, lipid metabolism, and branched-chain amino acid (BCAA) metabolism, and pointed to the complex pathogenesis mechanisms of APS and VTE.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!