Acute lung injury (ALI) is mainly caused by severe infection, shock, trauma, and burn, which causes the extensive release of inflammatory factors and other mediators. As a major bioactive constituent of traditional Chinese herb licorice, glycyrrhizic acid (GA) plays an important effect on inflammatory regulation. Nevertheless, the exact mechanism of this effect remains unclear. The present study aims to explore the potential protective effect of GA on LPS-induced ALI. Our results showed that GA significantly attenuated LPS-induced ALI and decreased the production of inflammatory factors, including IL-1β, MCP-1, COX2, HMGB1, and adhesion molecules, such as E-selectin, VCAM-1, and modulated expression of angiotensin-converting enzyme 2 (ACE2). Moreover, treatment of ACE2 inhibitor (MLN-4760) reversed the effects of GA on the secretion of pro-inflammatory factors in ALI. Additionally, GA exerts its protective effect by regulating the ACE2 and caveolin-1/NF-κB signaling pathway. In conclusion, this study showed that GA alleviated LPS-induced ALI by upregulating ACE2 and inhibiting the caveolin-1/NF-κB signaling pathway.

急性肺损伤（ALI）主要由严重感染、休克、创伤和烧伤引起，引起炎症因子等介质的广泛释放。作为中药甘草的主要生物活性成分，甘草酸（GA）对炎症调节具有重要作用。然而，这种效应的确切机制仍不清楚。本研究旨在探讨 GA 对 LPS 诱导的 ALI 的潜在保护作用。我们的研究结果表明，GA 显着减弱 LPS 诱导的 ALI 并减少炎症因子的产生，包括 IL-1β、MCP-1、COX2、HMGB1 和粘附分子，如 E-选择素、VCAM-1，并调节血管紧张素转换酶 2 (ACE2)。而且，ACE2 抑制剂 (MLN-4760) 的治疗逆转了 GA 对 ALI 中促炎因子分泌的影响。此外，GA 通过调节 ACE2 和caveolin-1/NF-κB 信号通路发挥其保护作用。总之，本研究表明，GA 通过上调 ACE2 和抑制caveolin-1/NF-κB 信号通路来缓解 LPS 诱导的 ALI。