Efficacy of methylprednisolone on T-2 toxin-induced cardiotoxicity in vivo: A pathohistological study

. 2019 Oct ; 71 () : 103221. [epub] 20190719

Jazyk angličtina Země Nizozemsko Médium print-electronic

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/pmid31365892
Odkazy

PubMed 31365892
DOI 10.1016/j.etap.2019.103221
PII: S1382-6689(19)30093-6
Knihovny.cz E-zdroje

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 < 0.01 vs. T-2 toxin). These changes were completely abolished by the therapeutic use of Lemod-solu® plus Lemod-depo® (p < 0.001 vs. T-2 toxin). Our results show that a significant cardioprotective efficacy of methylprednisolone is mediated by its anti-inflammatory activity.

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