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1,8-桉叶素可减轻脂多糖诱导的小鼠急性肺炎症。

1,8-cineol attenuates LPS-induced acute pulmonary inflammation in mice.

机构信息

Department of Pharmacology, Pharmacy and Biological Science College, Weifang Medical University, 7166 Baotong Street, Weifang, 261053, China,

出版信息

Inflammation. 2014 Apr;37(2):566-72. doi: 10.1007/s10753-013-9770-4.

Abstract

Eucalyptol, also known as 1,8-cineol, is a monoterpene and has been shown to exert anti-inflammatory and antioxidant effect. It is traditionally used to treat respiratory disorders due to its secretolytic properties. In the present study, we evaluated the effect of 1,8-cineol on pulmonary inflammation in a mouse model of acute lung injury. We found that 1,8-cineol significantly decreased the level of TNF-α and IL-1β, and increased the level of IL-10 in lung tissues after acute lung injury induced by lipopolysaccharide (LPS). It also reduced the expression of nuclear factor kappa B (NF-κB) p65 and toll-like receptor 4 (TLR4), and myeloperoxidase activity in lung tissues. In addition, 1,8-cineol reduced the amounts of inflammatory cells in bronchoalveolar lavage fluid (BALF), including neutrophils and macrophages, and significantly decreased the protein content in BALF and the lung wet/dry weight (W/D) ratio. Its effect on LPS-induced pulmonary inflammation was associated with suppression of TLR4 and NF-κB expressions. Our results provide evidence that 1,8-cineol inhibits acute pulmonary inflammation, indicating its potential for the treatment of acute lung injury.

摘要

桉油醇,又称 1,8-桉叶素,是一种单萜类化合物,具有抗炎和抗氧化作用。因其具有溶解分泌物的特性,传统上被用于治疗呼吸道疾病。在本研究中,我们评估了 1,8-桉叶醇对脂多糖(LPS)诱导的急性肺损伤小鼠模型中肺部炎症的影响。我们发现,1,8-桉叶醇可显著降低 LPS 诱导的急性肺损伤后肺组织中 TNF-α 和 IL-1β 的水平,并增加 IL-10 的水平。它还降低了肺组织中核因子 κB(NF-κB)p65 和 Toll 样受体 4(TLR4)的表达以及髓过氧化物酶的活性。此外,1,8-桉叶醇还减少了支气管肺泡灌洗液(BALF)中炎性细胞的数量,包括中性粒细胞和巨噬细胞,并显著降低了 BALF 中的蛋白含量和肺湿/干重(W/D)比。其对 LPS 诱导的肺部炎症的作用与 TLR4 和 NF-κB 表达的抑制有关。我们的结果提供了证据表明,1,8-桉叶醇抑制急性肺部炎症,表明其在治疗急性肺损伤方面具有潜力。

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