卡托普利降低小鼠模型的chabaudi疟原虫感染肝细胞毒性

IF 4.2 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES
Priscilla Dantas de Souza Ventura , Daniel Vitor de Souza , Anna Caroline C. Aguiar , Carolina P.F. Carvalho , Daniel A. Ribeiro , Marcia R. Nagaoka , Marcos L. Gazarini
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引用次数: 0

摘要

疟原虫属负责疟疾感染,并促进血色素的积累,随后在肝脏中产生氧化性物质,这涉及肝损伤。在此背景下,我们用抗疟药氯喹、卡托普利(ACE I抑制剂)、氯沙坦(AT1受体阻滞剂)口服治疗感染chabaudi疟原虫的小鼠肝脏进行了组织病理学分析。在苏木精和伊红染色的肝脏切片上,组织病理学变化,如窦充血、白细胞浸润、血色素沉积、门道炎症和元核分析进行了评估。组织病理学分析显示,单独使用氯喹或联合使用血管扩张剂治疗有益,减少了每次组织变化的评分。我们的数据显示,chabaudi疟原虫感染损害了一些肝脏组织病理学参数,有趣的是,血管扩张剂治疗改善了这些改变。特别是,卡托普利降低疟疾感染引起的小鼠肝细胞毒性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Captopril reduces liver cytotoxicity in a murine model of Plasmodium chabaudi infection
The genus Plasmodium is responsible for malaria infection and promoting an accumulation of hemozoin followed by the generation of oxidizing species in the liver that is involved in hepatic damage. In this context, we performed the histopathological analysis in the mice liver infected with Plasmodium chabaudi treated orally with the antimalarial chloroquine, captopril (ACE I inhibitor), losartan (AT1 receptor blocker). In hematoxylin and eosin-stained liver sections, histopathological changes, such as sinusoid congestion, leukocyte infiltration, hemozoin deposition, portal tract inflammation, and metanuclear analysis were evaluated. The histopathological analysis shows a beneficial effect of chloroquine treatment alone or in combination with vasodilator treatments, reducing the score for each tissue change. Our data show that Plasmodium chabaudi infection compromises some hepatic histopathological parameters, and interestingly the treatment with vasodilators improved some of these alterations. Particularly, captopril reduces cytotoxicity induced by malaria infection in mouse liver cells.
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来源期刊
CiteScore
7.00
自引率
4.70%
发文量
185
审稿时长
34 days
期刊介绍: Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.
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