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甘草酸通过下调肺泡巨噬细胞中的TLR2信号级联反应改善缺血再灌注肺损伤。

Glycyrrhizin Ameliorate Ischemia Reperfusion Lung Injury through Downregulate TLR2 Signaling Cascade in Alveolar Macrophages.

作者信息

Fei Lin, Jifeng Feng, Tiantian Wang, Yi He, Linghui Pan

机构信息

Department of Anesthesiology, Affiliated Tumor Hospital of Guangxi Medical UniversityNanning, China.

Department of Anesthesiology, Guangxi Maternal and Child Health HospitalNanning, China.

出版信息

Front Pharmacol. 2017 Jun 16;8:389. doi: 10.3389/fphar.2017.00389. eCollection 2017.

DOI:10.3389/fphar.2017.00389
PMID:28670282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5472719/
Abstract

This experiment was conducted to study whether pretreatment with Glycyrrhizin (GL) could ameliorate ischemia-reperfusion (I/R) lung injury and investigate the mechanisms of its protective effects in a mice model. Six-eight weeks male BALB/C mice were randomly assigned to four groups ( = 6): Control, Glycyrrhizin, I/R and I/R+Glycyrrhizin. Lung I/R was achieved by clamping the left hilus pulmonis. GL (200 mg/kg) was injected intraperitoneally 30 min before anesthesia. Measurement of pathohistological lung injury score, pulmonary permeability, isolated alveolar macrophages, inflammatory mediators, TLR2 and its downstream factors (MyD88, NF-κB) were performed. The results were as anticipated. Pathohistological evaluation indicated that GL significantly ameliorated I/R-induced lung injury, pulmonary permeability and edema. Pretreatment with GL significantly inhibited I/R-induced inflammation in lung tissues and BALF. In addition, GL significantly decreased I/R-induced isolated alveolar macrophages and suppressed I/R-induced expression of TLR2 and its downstream factors in lung tissues and alveolar macrophages. Collectively, our data indicated that pretreatment with GL could ameliorate I/R lung injury. The mechanisms of its protective effects might be inhibit I/R-induced inflammatory response through downregulate TLR2 signaling cascade in alveolar macrophages.

摘要

本实验旨在研究甘草酸（GL）预处理是否能改善缺血再灌注（I/R）肺损伤，并在小鼠模型中探讨其保护作用机制。将6-8周龄雄性BALB/C小鼠随机分为四组（每组n = 6）：对照组、甘草酸组、I/R组和I/R+甘草酸组。通过夹闭左肺门实现肺I/R。在麻醉前30分钟腹腔注射GL（200 mg/kg）。进行肺组织病理损伤评分、肺通透性、分离的肺泡巨噬细胞、炎症介质、TLR2及其下游因子（MyD88、NF-κB）的检测。结果符合预期。组织病理学评估表明，GL显著改善了I/R诱导的肺损伤、肺通透性和水肿。GL预处理显著抑制了I/R诱导的肺组织和支气管肺泡灌洗液（BALF）中的炎症。此外，GL显著减少了I/R诱导的分离肺泡巨噬细胞，并抑制了I/R诱导的肺组织和肺泡巨噬细胞中TLR2及其下游因子的表达。总体而言，我们的数据表明，GL预处理可改善I/R肺损伤。其保护作用机制可能是通过下调肺泡巨噬细胞中的TLR2信号级联反应来抑制I/R诱导的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/ffe8ccce96c9/fphar-08-00389-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/26b039a3dd56/fphar-08-00389-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/d227d500824e/fphar-08-00389-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/6e7d5b774a7a/fphar-08-00389-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/91a1c4e5dce4/fphar-08-00389-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/ffe8ccce96c9/fphar-08-00389-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/26b039a3dd56/fphar-08-00389-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/d227d500824e/fphar-08-00389-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/d91d0dc1d1c0/fphar-08-00389-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/6e7d5b774a7a/fphar-08-00389-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/91a1c4e5dce4/fphar-08-00389-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a84/5472719/ffe8ccce96c9/fphar-08-00389-g006.jpg

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