Affiliations 

  • 1 National Poison Control Centre, Military Medical Academy, 17 Crnotravska St, 11000, Belgrade, Serbia; Medical Faculty of the Military Medical Academy, University of Defence, 1 Pavla Jurišića-Šturma St, 11000, Belgrade, Serbia; Department of Chemistry, Faculty of Science, University of Hradec Kralove, Rokitanského 62, 500 03, Hradec Králové, Czechia
  • 2 College of Life Science, Yangtze University, 1 Nanhuan Road, 434023, Jingzhou, Hubei, China; Department of Chemistry, Faculty of Science, University of Hradec Kralove, Rokitanského 62, 500 03, Hradec Králové, Czechia
  • 3 Department of Chemistry, Faculty of Science, University of Hradec Kralove, Rokitanského 62, 500 03, Hradec Králové, Czechia
  • 4 Department of Chemistry, Faculty of Science, University of Hradec Kralove, Rokitanského 62, 500 03, Hradec Králové, Czechia; Malaysia-Japan International Institute of Technology (MJIIT), University Teknologi Malaysia, Jalan Sultan Yahya Petra, 54100, Kuala Lumpur, Malaysia. Electronic address: kamil.kuca@uhk.cz
Environ Toxicol Pharmacol, 2019 Oct;71:103221.
PMID: 31365892 DOI: 10.1016/j.etap.2019.103221

Abstract

Our aim was to compare the protective efficacy of two different formulations of methylprednisolone in T-2 toxin-induced cardiomyopathy. Methylprednisolone (soluble form, Lemod-solu® and/or depot form, Lemod-depo®, a total single dose of 40 mg/kg im) was given immediately after T-2 toxin (1 LD50 0.23 mg/kg sc). The myocardial tissue samples were examinated by using histopathology, semiquantitative and imaging analyses on day 1, 7, 14, 21, 28 and 60 of the study. Therapeutic application of Lemod-solu® significantly decreased the intensity of myocardial degeneration and haemorrhages, distribution of glycogen granules in the endo- and perimysium, a total number of mast cells and the degree of their degranulation was in correlation with the reversible heart structural lesions (p 

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.