Astragalin attenuates lipopolysaccharide-induced inflammatory responses by down-regulating NF-魏B signaling pathway

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• 作者：Lanan Wassy Soromou^a ; Na Chen^a ; Lanxiang Jiang^b ; Meixia Huo^a ; Miaomiao Wei^a ; Xiao Chu^a ; Faya Martin Millimouno^c ; Haihua Feng^a ; Youssouf Sidime^c ; ^{adamformationujk@hotmail.fr} ; Xuming Deng^a ; ^{xumingdeng@jluhp.edu.cn} ; ^{ysfprof@yahoo.com}
• 关键词：Astragalin ; Lipopolysaccharide ; Inflammatory responses ; Cytokine ; Endotoxemia ; Acute lung injury
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 期刊代码：159_0006291x
• 类别：bio
• 出版时间：9 March, 2012
• 卷：419
• 期：2
• 页码：256-261
• 文件大小：921 K

摘要

Astragalin (AG), a flavonoid from many traditional herbs and medicinal plants, has been described to exhibit in vitro anti-inflammatory activity. The present study aimed to determine the protective effects and the underlying mechanisms of astragalin on lipopolysaccharide-induced endotoxemia and lung injury in mice. Mice were injected intraperitoneally (i.p.) with lipopolysaccharide (LPS) (dose range: 5-40 mg/kg). We observed mice on mortality for 7 days twice a day and recorded survival rates. In drug testing, we examined the therapeutic effects of astragalin (25, 50 or 75 mg/kg) on LPS- induced endotoxemia by dosing orally astragalin 1 hour before LPS challenge. Using an experimental model of LPS-induced acute lung injury (ALI), we examined the effect of astragalin in resolving lung injury. The investigations revealed that pretreatment with astragalin can improve survival during lethal endotoxemia and attenuate inflammatory responses in a murine model of lipopolysaccharide-induced acute lung injury. The mechanisms by which Astragalin exerts its anti-inflammatory effect are correlated with inhibition of tumor necrosis factor-伪 (TNF-伪), interleukin-1 (IL-1), and interleukin-6 (IL-6) production via inactivation of NF-魏B.