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
{"title":"卡托普利降低小鼠模型的chabaudi疟原虫感染肝细胞毒性","authors":"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","doi":"10.1016/j.etap.2025.104801","DOIUrl":null,"url":null,"abstract":"<div><div>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 <em>Plasmodium chabaudi</em> 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 <em>Plasmodium chabaudi</em> 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.</div></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"119 ","pages":"Article 104801"},"PeriodicalIF":4.2000,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Captopril reduces liver cytotoxicity in a murine model of Plasmodium chabaudi infection\",\"authors\":\"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\",\"doi\":\"10.1016/j.etap.2025.104801\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>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 <em>Plasmodium chabaudi</em> 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 <em>Plasmodium chabaudi</em> 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.</div></div>\",\"PeriodicalId\":11775,\"journal\":{\"name\":\"Environmental toxicology and pharmacology\",\"volume\":\"119 \",\"pages\":\"Article 104801\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2025-08-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Environmental toxicology and pharmacology\",\"FirstCategoryId\":\"93\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1382668925001760\",\"RegionNum\":3,\"RegionCategory\":\"环境科学与生态学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENVIRONMENTAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Environmental toxicology and pharmacology","FirstCategoryId":"93","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1382668925001760","RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
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.
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.