甲泼尼龙对 T-2 毒素体内诱导的心脏毒性的疗效：一项病理组织学研究。

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

机构信息

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.

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.

出版信息

Environ Toxicol Pharmacol. 2019 Oct;71:103221. doi: 10.1016/j.etap.2019.103221. Epub 2019 Jul 19.

DOI:10.1016/j.etap.2019.103221

PMID:31365892

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 LD 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.

摘要

我们的目的是比较两种不同剂型的甲泼尼龙在 T-2 毒素诱导的心肌病中的保护效果。甲泼尼龙（可溶性形式，Lemod-solu 和/或长效形式，Lemod-depo，总剂量为 40mg/kg 肌内注射）在 T-2 毒素（1LD 0.23mg/kg 皮下注射）后立即给予。在研究的第 1、7、14、21、28 和 60 天，通过组织病理学、半定量和成像分析检查心肌组织样本。Lemod-solu 的治疗应用显著降低了心肌变性和出血的强度、内和外肌膜间糖原颗粒的分布、肥大细胞的总数及其脱颗粒的程度，与可逆性心脏结构损伤相关（p<0.01 与 T-2 毒素相比）。Lemod-solu 联合 Lemod-depo 的治疗应用完全消除了这些变化（p<0.001 与 T-2 毒素相比）。我们的结果表明，甲泼尼龙的显著心脏保护作用是通过其抗炎活性介导的。