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紫丁香苷对脂多糖诱导的小鼠急性肺损伤的保护作用。

Protective effects of syringin against lipopolysaccharide-induced acute lung injury in mice.

作者信息

Zhang Ao, Liu Zhongmin, Sheng Lulu, Wu Hui

机构信息

Department of Intensive Care Unit, First Hospital of Jilin University, Changchun, China.

Department of Ophthalmology, First Hospital of Jilin University, Changchun, China.

出版信息

J Surg Res. 2017 Mar;209:252-257. doi: 10.1016/j.jss.2016.10.027. Epub 2016 Nov 5.

DOI:10.1016/j.jss.2016.10.027
PMID:28032567
Abstract

BACKGROUND

Syringin, a major active substance isolated from Eleutherococcus senticosus, has been found to have anti-inflammatory effect. The aim of this study was to investigate the effects and underlying mechanisms of syringin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.

METHODS

We established an LPS-induced ALI model in mice. We also detected the lung wet-to-dry ratio, myeloperoxidase activity, and inflammatory cytokines tumor necrosis factor alpha, interleukin (IL)-1β, and IL-6 to estimate the index of lung injury in mice. Furthermore, the expression of nuclear factor-erythroid 2-related factor-2 (Nrf2), heme oxygenase-1, and nuclear factor κB (NF-κB) was detected by Western blot analysis.

RESULTS

The results showed that the increases in lung wet-to-dry ratio, myeloperoxidase activity, malondialdehyde content, and levels of tumor necrosis factor alpha, IL-1β, and IL-6 induced by LPS were significantly inhibited by treatment of syringin. The phosphorylation of IκB-α and p65 NF-κB caused by LPS was inhibited by syringin. Furthermore, syringin was found to upregulate the expression of Nrf2 and heme oxygenase 1.

CONCLUSIONS

In conclusion, the results suggest that syringin protects against LPS-induced ALI by activating Nrf2 and inhibiting NF-κB signaling pathway.

摘要

背景

紫丁香苷是从刺五加中分离出的一种主要活性物质,已被发现具有抗炎作用。本研究旨在探讨紫丁香苷对脂多糖(LPS)诱导的小鼠急性肺损伤(ALI)的影响及潜在机制。

方法

我们建立了LPS诱导的小鼠ALI模型。我们还检测了肺组织湿干比、髓过氧化物酶活性以及炎性细胞因子肿瘤坏死因子α、白细胞介素(IL)-1β和IL-6,以评估小鼠肺损伤指标。此外,通过蛋白质免疫印迹分析检测核因子红系2相关因子2(Nrf2)、血红素加氧酶-1和核因子κB(NF-κB)的表达。

结果

结果显示,紫丁香苷处理可显著抑制LPS诱导的肺湿干比、髓过氧化物酶活性、丙二醛含量以及肿瘤坏死因子α、IL-1β和IL-6水平的升高。紫丁香苷可抑制LPS引起的IκB-α和p65 NF-κB的磷酸化。此外,发现紫丁香苷可上调Nrf2和血红素加氧酶1的表达。

结论

总之,结果表明紫丁香苷通过激活Nrf2和抑制NF-κB信号通路来保护小鼠免受LPS诱导的ALI。

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