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蒲公英甾醇通过抑制活性氧诱导的Toll样受体4(TLR4)向脂筏的转运来抑制香烟烟雾诱导的肺部炎症。

Taraxasterol inhibits cigarette smoke-induced lung inflammation by inhibiting reactive oxygen species-induced TLR4 trafficking to lipid rafts.

作者信息

Xueshibojie Liu, Duo Yu, Tiejun Wang

机构信息

Department of Otolaryngology Head and Neck Surgery, 2nd Hospital Affiliated of Jilin University, Changchun, Jilin Province 130041, China.

Department of Radiotherapy, 2nd Hospital Affiliated of Jilin University, Changchun, Jilin Province 130041, China.

出版信息

Eur J Pharmacol. 2016 Oct 15;789:301-307. doi: 10.1016/j.ejphar.2016.07.047. Epub 2016 Jul 28.

DOI:10.1016/j.ejphar.2016.07.047
PMID:27477353
Abstract

Taraxasterol, a pentacyclic-triterpene isolated from Taraxacum officinale, has been demonstrated to have anti-inflammatory effects. However, the protective effects of taraxasterol against cigarette smoke (CS)-induced lung inflammation have not been reported. This study aimed to investigate the protective effects and mechanism of taraxasterol on CS-induced lung inflammation in mice. CS-induced mouse lung inflammation model was used to investigate the protective effects of taraxasterol in vivo. Human bronchial epithelial cells (HBECs) were used to investigate the protective mechanism of taraxasterol in vitro. The results showed that taraxasterol attenuated CS-induced lung pathological changes, inflammatory cells infiltration, inflammatory cytokines TNF-α, IL-6 and IL-1β production. Taraxasterol also up-regulated CS-induced glutathione (GSH) production. In vitro, taraxasterol was found to inhibit CS-induced reactive oxygen species production, recruitment of TLR4 into lipid rafts, NF-κB activation, and IL-8 production. Furthermore, our results showed that antioxidant N-acetyl-L-cysteine (NAC) significantly inhibited CS-induced recruitment of TLR4 into lipid rafts as well as IL-8 production. In conclusion, our results suggested that taraxasterol had protective effects of CS-induced lung inflammation.

摘要

蒲公英甾醇是一种从蒲公英中分离出的五环三萜,已被证明具有抗炎作用。然而,蒲公英甾醇对香烟烟雾(CS)诱导的肺部炎症的保护作用尚未见报道。本研究旨在探讨蒲公英甾醇对CS诱导的小鼠肺部炎症的保护作用及其机制。采用CS诱导的小鼠肺部炎症模型研究蒲公英甾醇在体内的保护作用。用人支气管上皮细胞(HBECs)研究蒲公英甾醇在体外的保护机制。结果表明,蒲公英甾醇减轻了CS诱导的肺部病理变化、炎症细胞浸润、炎症细胞因子TNF-α、IL-6和IL-1β的产生。蒲公英甾醇还上调了CS诱导的谷胱甘肽(GSH)的产生。在体外,发现蒲公英甾醇可抑制CS诱导的活性氧产生、TLR4募集到脂筏、NF-κB激活和IL-8产生。此外,我们的结果表明,抗氧化剂N-乙酰-L-半胱氨酸(NAC)显著抑制CS诱导的TLR4募集到脂筏以及IL-8产生。总之,我们的结果表明蒲公英甾醇对CS诱导的肺部炎症具有保护作用。

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