血管紧张素II型2受体激活可减轻慢性空气污染引起的炎症和氧化应激

IF 4.2 3区环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES

Environmental toxicology and pharmacology Pub Date : 2025-08-26 DOI:10.1016/j.etap.2025.104800

Jorge A. Narvaez Pardo , Agustina Freire , Marina C. Muñoz , Bruno Buchholz , Analía L. Tomat , Mariela M. Gironacci , Ulrike M. Steckelings , Natalia D. Magnani , Pablo A. Evelson , Fernando P. Dominici

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引用次数: 0

摘要

在暴露于城市空气（UA） 14周的小鼠模型中，评估了慢性暴露于城市空气（UA）对肾素-血管紧张素系统（RAS）成分的影响，以及血管紧张素2型受体（AT2R）激动剂化合物21 （C21）减轻污染引起的炎症和氧化应激的治疗潜力。暴露于空气污染中会增加肺和肾脏的促炎细胞因子和氧化损伤标志物，并上调血管紧张素转换酶；ACE和血管紧张素1型受体；肺中的AT1R；同时诱导Mas受体代偿性增加；心脏和肾脏的MasR和AT2R。C21治疗可降低肺组织中IL-1β和TNF-α的表达以及肺和肾组织中3-硝基酪氨酸的水平，下调肺组织中ACE和AT1R的表达，增加肾组织中MasR的表达。目前的结果强调了RAS失调在污染诱导的组织损伤中的相关性，并将AT2R激动剂作为减轻空气污染对健康影响的一种可能性。

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Angiotensin II type 2 receptor activation alleviates inflammation and oxidative stress caused by chronic exposure to air pollution

The impact of chronic exposure to urban air (UA) on renin-angiotensin system (RAS) components and the therapeutic potential of the angiotensin type 2 receptor (AT₂R) agonist, Compound 21 (C21), in mitigating pollution-induced inflammation and oxidative stress was evaluated in a mouse model exposed to UA for 14 weeks. Air pollution exposure increased pro-inflammatory cytokines and oxidative damage markers in the lungs and kidneys and upregulated angiotensin converting enzyme; ACE, and angiotensin type 1 receptor; AT₁R in the lungs; while it induced a compensatory increase in Mas receptor; MasR and AT₂R in the heart and kidneys. C21 treatment reduced IL-1β and TNF-α expression in the lungs and 3-nitrotyrosine levels in the lungs and kidneys, downregulated both ACE and AT₁R expression in the lungs and increased renal MasR expression. Current results underscore the relevance of RAS dysregulation in pollution-induced tissue damage and positions AT₂R agonism as a possibility for mitigating the health impacts of air pollution.

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来源期刊

Environmental toxicology and pharmacology 医学-毒理学

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.