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Anti-inflammatory and antioxidant effects of the nanocomposite Fullerol decrease the severity of intestinal inflammation induced by gut ischemia and reperfusion

活性氧 肠系膜上动脉 缺血 固有层 炎症 再灌注损伤 肠粘膜 化学 药理学 氧化应激 外渗 免疫学 医学 病理 内科学 生物化学 上皮
作者
Raquel Duque do Nascimento Arifa,Talles Prosperi de Paula,Renata Lacerda Lima,Camila B. Brito,Maria Emília Rabelo Andrade,Valbert Nascimento Cardoso,M. V. B. Pinheiro,Luiz O. Ladeira,Klaus Krambrock,Mauro M. Teixeira,Caio T. Fagundes,Danielle G. Souza
出处
期刊:European Journal of Pharmacology [Elsevier]
卷期号:898: 173984-173984 被引量:9
标识
DOI:10.1016/j.ejphar.2021.173984
摘要

Intestinal ischemia is a vascular emergency that arises when blood flow to the intestine is compromised. Reperfusion is necessary to restore intestinal function but might lead to local and systemic inflammatory responses and bacterial translocation, with consequent multiple organ dysfunction syndrome (MODS). During reperfusion occurs production of reactive oxygen species. These species contribute to intestinal injury through direct toxicity or activation of inflammatory pathways. Fullerol is a nanacomposite which has been shown to act as reactive oxygen species and reactive nitrogen species (RNS) scavengers. Thus, our aim was to evaluate whether Fullerol confer anti-inflammatory activity during intestinal ischemia and reperfusion (IIR). Intestinal ischemia was induced by total occlusion of the superior mesenteric artery. Groups were treated with vehicle or Fullerol 10 min before reperfusion. Mice were euthanized after 6 h of reperfusion, and small intestines were collected for evaluation of plasma extravasation, leukocyte influx, cytokine production and histological damage. Bacterial translocation to the peritoneal cavity and reactive oxygen and nitrogen species production by lamina propria cells were also evaluated. Our results showed that treatment with Fullerol inhibited bacterial translocation to the peritoneal cavity, delayed and decreased the lethality rates and diminished neutrophil influx and intestinal injury induced by IIR. Reduced severity of reperfusion injury in Fullerol-treated mice was associated with blunted reactive oxygen and nitrogen species production in leukocytes isolated from gut lamina propria and decreased production of pro-inflammatory mediators. Thus, the present study shows that Fullerol is a potential therapy to treat inflammatory bowel disorders associated with bacterial translocation, such as IIR.
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