Glycyrrhizin Ameliorate Ischemia Reperfusion Lung Injury through Downregulate TLR2 Signaling Cascade in Alveolar Macrophages.
Glycyrrhizin Ameliorate Ischemia Reperfusion Lung Injury through Downregulate TLR2 Signaling Cascade in Alveolar Macrophages.
复制标题
甘草酸通过下调肺泡巨噬细胞中的 TLR2 信号级联减轻缺血再灌注肺损伤
DOI：
10.3389/fphar.2017.00389
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发表时间：
2017-01-01
影响因子：
5.6
通讯作者：
Linghui, Pan
中科院分区：
文献类型：
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作者：
Fei, Lin;Jifeng, Feng;Linghui, Pan
本实验采用小鼠肺缺血再灌注（I/R）模型，研究甘草酸（GL）预处理对I/R肺损伤的保护作用及其机制。将6 - 8周龄雄性BALB/C小鼠随机分为4组（n = 6）：对照组、甘草甜素组、I/R组和I/R+甘草甜素组。通过夹闭左肺门实现肺I/R。麻醉前30 min腹腔注射GL（200 mg/kg）。检测肺组织病理损伤评分、肺通透性、肺泡巨噬细胞、炎症介质、TLR 2及其下游因子（MyD 88、NF-κB B）。结果如预期。病理组织学观察表明，GL可明显减轻I/R所致的肺损伤、肺通透性和肺水肿。GL预处理可显著抑制I/R诱导的肺组织和BALF炎症反应。此外，GL还能显著降低I/R诱导的肺泡巨噬细胞数量，抑制I/R诱导的肺组织和肺泡巨噬细胞TLR 2及其下游因子的表达。总的来说，我们的数据表明，GL预处理可以减轻I/R肺损伤。其机制可能是通过下调肺泡巨噬细胞TLR 2信号通路抑制I/R诱导的炎症反应。
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 (n = 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.