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丁香酚的抗炎和抗氧化作用可改善脂多糖诱导的肺损伤。

The anti-inflammatory and anti-oxidative actions of eugenol improve lipopolysaccharide-induced lung injury.

作者信息

Magalhães Clarissa B, Casquilho Nathalia V, Machado Mariana N, Riva Douglas R, Travassos Leonardo H, Leal-Cardoso José Henrique, Fortunato Rodrigo S, Faffe Débora S, Zin Walter A

机构信息

Laboratory of Respiration Physiology, Carlos Chagas Filho Institute of Biophysics, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

Superior Institute of Biomedical Sciences, Ceara State University, Fortaleza, Brazil.

出版信息

Respir Physiol Neurobiol. 2019 Jan;259:30-36. doi: 10.1016/j.resp.2018.07.001. Epub 2018 Jul 8.

DOI:10.1016/j.resp.2018.07.001
PMID:29997055
Abstract

Acute lung injury (ALI) remains a major cause of mortality. In lipopolysaccharide (LPS)-stimulated macrophages, eugenol reduces cyclooxygenase-2 expression, NF-κB activation, and inflammatory mediators. We examined the anti-inflammatory and anti-oxidative action of eugenol in an in vivo model of LPS-induced lung injury. Lung mechanics and histology were analyzed in mice 24 h after LPS exposure, with and without eugenol treatment at different doses. Additional animals, submited to the same protocol, were treated with eugenol at 150 mg/kg to determine its effect on inflammatory cytokines (ELISA) and oxidative markers. LPS-induced lung functional and histological changes were significantly improved by eugenol, in a dose-dependent way. Furthermore, eugenol (150 mg/kg) was able to inhibit the release of inflammatory cytokines (TNF-α, IL-1β and IL-6), NADPH oxidase activity, as well as antioxidant enzymes activity (superoxide dismutase, catalase and glutathione peroxidase). Finally, eugenol reduced LPS-induced protein oxidation. In conclusion, eugenol improved in vivo LPS-induced ALI through both anti-inflammatory and anti-oxidative effects, avoiding damage to lung structure.

摘要

急性肺损伤(ALI)仍然是主要的死亡原因。在脂多糖(LPS)刺激的巨噬细胞中,丁香酚可降低环氧合酶-2的表达、NF-κB的激活以及炎症介质的产生。我们在LPS诱导的肺损伤体内模型中研究了丁香酚的抗炎和抗氧化作用。在暴露于LPS 24小时后的小鼠中,分析了有无不同剂量丁香酚治疗情况下的肺力学和组织学情况。按照相同方案对另外的动物给予150 mg/kg丁香酚治疗,以确定其对炎症细胞因子(酶联免疫吸附测定)和氧化标志物的影响。丁香酚以剂量依赖的方式显著改善了LPS诱导的肺功能和组织学变化。此外,丁香酚(150 mg/kg)能够抑制炎症细胞因子(肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-6)的释放、NADPH氧化酶活性以及抗氧化酶活性(超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶)。最后,丁香酚减少了LPS诱导的蛋白质氧化。总之,丁香酚通过抗炎和抗氧化作用改善了体内LPS诱导的ALI,避免了肺结构的损伤。

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