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通过调节Toll样受体4/核因子-κB信号通路改善脂多糖诱导的大鼠急性肺损伤

and Ameliorate Lipopolysaccharide-Induced Acute Lung Injury in Rats by Regulating the Toll-Like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway.

作者信息

Qin Li, Tan Hong-Ling, Wang Yu-Guo, Xu Cheng-Yong, Feng Jian, Li Min, Dou Yong-Qi

机构信息

Department of Traditional Chinese Medicine, Chinese PLA General Hospital, Beijing 100853, China.

Institute of Radiation Medicine Sciences, Academy of Military Medical Sciences, Beijing 100850, China.

出版信息

Evid Based Complement Alternat Med. 2018 Jan 29;2018:3017571. doi: 10.1155/2018/3017571. eCollection 2018.

DOI:10.1155/2018/3017571
PMID:29619068
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5829314/
Abstract

and (AM/SM) are well used in Traditional Chinese Medicines (TCM) for nourishing Qi and activating blood circulation method. From TCM theory, the pathogenesis of acute lung injury (ALI) was determined as Qi deficiency and blood stagnation. In this study, we are aiming to investigate the protective and therapeutic effects of AM/SM on a rat model of lipopolysaccharide- (LPS-) induced ALI in rats and to elucidate potential molecular mechanisms. ALI was induced by intratracheal instillation of LPS (5 mg/kg) in Sprague-Dawley rats. SM/AM was given orally before and after LPS administration. Results demonstrated that AM/SM attenuated lung histopathological changes induced by LPS, decreased wet/dry weight ratios and protein concentrations, and inhibited the production of tumor necrosis factor-alpha (TNF-) and interleukin-6 (IL-6) in BALF. Moreover, AM/SM significantly downregulated protein and mRNA expression of toll-like receptors 4 (TLR-4), interleukin-1 receptor-associated kinase-1 (IRAK-1), and nuclear factor-kappa B (NF-B/p65). These findings suggest that AM/SM showed protective and therapeutic effects in LPS-induced ALI rat through modulating TLR-4 signaling pathways. Nourishing Qi and activating blood circulation may be a beneficial treatment for ALI.

摘要

黄芪甲苷（AM）和丹参酮ⅡA（SM）在传统中药中常用于益气活血法。从中医理论来看，急性肺损伤（ALI）的发病机制被确定为气虚血瘀。在本研究中，我们旨在探讨AM/SM对脂多糖（LPS）诱导的大鼠ALI模型的保护和治疗作用，并阐明潜在的分子机制。通过向Sprague-Dawley大鼠气管内滴注LPS（5mg/kg）诱导ALI。在LPS给药前后口服SM/AM。结果表明，AM/SM减轻了LPS诱导的肺组织病理学变化，降低了湿/干重比和蛋白质浓度，并抑制了支气管肺泡灌洗液（BALF）中肿瘤坏死因子-α（TNF-）和白细胞介素-6（IL-6）的产生。此外，AM/SM显著下调了Toll样受体4（TLR-4）、白细胞介素-1受体相关激酶-1（IRAK-1）和核因子-κB（NF-κB/p65）的蛋白和mRNA表达。这些发现表明，AM/SM通过调节TLR-4信号通路对LPS诱导的ALI大鼠具有保护和治疗作用。益气活血可能是ALI的一种有益治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/fa3faa06e1a6/ECAM2018-3017571.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/5bcc7de2a01c/ECAM2018-3017571.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/74de599d0fef/ECAM2018-3017571.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/45650b6c5834/ECAM2018-3017571.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/2c41be28d042/ECAM2018-3017571.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/d324896e9b6a/ECAM2018-3017571.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/b80e578f4864/ECAM2018-3017571.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/fa3faa06e1a6/ECAM2018-3017571.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/5bcc7de2a01c/ECAM2018-3017571.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/74de599d0fef/ECAM2018-3017571.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/45650b6c5834/ECAM2018-3017571.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/2c41be28d042/ECAM2018-3017571.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/d324896e9b6a/ECAM2018-3017571.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/b80e578f4864/ECAM2018-3017571.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2468/5829314/fa3faa06e1a6/ECAM2018-3017571.007.jpg

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