Long Kaihua, Yang Yun, Wang Yuan, Wang Bo, Zhou Huiying, Liu Yuxi, Li Ye, Yang Shuanzhu, Cao Liping, Huang Tingting, Liu Yang, Zhang Hong
Shaanxi Academy of Traditional Chinese Medicine (Shaanxi Provincial Hospital of Traditional Chinese Medicine), Xi'an, People's Republic of China.
College of Life Sciences, Northwest University, Xi'an, People's Republic of China.
J Inflamm Res. 2025 Aug 4;18:10425-10443. doi: 10.2147/JIR.S523490. eCollection 2025.
Currently, clinical treatments for ALI include vasodilators, glucocorticoids, and mechanical ventilation; however, these therapies are associated with various adverse reactions. Therefore, there is a need to develop safer and more effective treatment options. Traditional Chinese Medicine (TCM), particularly Qingwen Hufei Granules (QHG), has demonstrated efficacy in treating respiratory disorders, including upper respiratory tract infections and influenza. However, the active components and mechanism of action of QHG remain unclear.
Lipopolysaccharide (LPS) induced ALI mouse model. We analyzed the main pharmacodynamic components of QHG by HPLC, determined the effects of QHG on the cell viability and inflammatory factors of RAW264.7 cells, and recorded the body weight and lung tissue wet/dry (W/D) of ALI mice. Inflammatory factors in bronchoalveolar lavage fluid (BALF), serum, and lung tissue were determined using ELISA, and the protective effect of hematoxylin and eosin (H&E) staining of lung tissue was studied. Transcriptomic, qRT-PCR, Western blotting, immunohistochemistry, and immunofluorescence analyses were used to analyze QHG and explore the mechanism of ALI damage reduction.
The findings demonstrated that QHG effectively mitigated inflammatory cell invasion and pulmonary edema. Moreover, it diminished the concentrations of IL-6, TNF-α, and IL-1β in lung tissue, serum, and BALF. Furthermore, QHG notably decreased the levels of NO, reactive oxygen species(ROS), IL-6, IL-1β, and TNF-α in the supernatants of RAW264.7 cells. Transcriptomic analysis of the lung tissue revealed that QHG primarily enriched the NOD-like receptor (NLR) signaling pathway. qRT-PCR, Western blotting, immunohistochemistry, and immunofluorescence experiments confirmed that QHG mitigated ALI damage through the NLR signaling pathway. Furthermore, seven key components in QHG were determined by using HPLC.
Our study demonstrated that QHG effectively mitigated LPS-induced ALI, and provided preliminary insights into its mechanism of action and material basis.
目前，急性肺损伤（ALI）的临床治疗方法包括使用血管扩张剂、糖皮质激素和机械通气；然而，这些疗法都伴有各种不良反应。因此，有必要开发更安全、更有效的治疗方案。传统中医药（TCM），特别是清瘟护肺颗粒（QHG），已证明在治疗包括上呼吸道感染和流感在内的呼吸系统疾病方面具有疗效。然而，QHG的活性成分和作用机制仍不清楚。
采用脂多糖（LPS）诱导ALI小鼠模型。我们通过高效液相色谱法（HPLC）分析了QHG的主要药效成分，测定了QHG对RAW264.7细胞活力和炎症因子的影响，并记录了ALI小鼠的体重和肺组织湿/干重（W/D）。使用酶联免疫吸附测定（ELISA）法测定支气管肺泡灌洗液（BALF）、血清和肺组织中的炎症因子，并研究苏木精-伊红（H&E）染色对肺组织的保护作用。采用转录组学、定量逆转录聚合酶链反应（qRT-PCR）、蛋白质免疫印迹法（Western blotting）、免疫组织化学和免疫荧光分析来分析QHG并探索其减轻ALI损伤的机制。
研究结果表明，QHG有效地减轻了炎症细胞浸润和肺水肿。此外，它降低了肺组织、血清和BALF中白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）的浓度。此外，QHG显著降低了RAW264.7细胞上清液中一氧化氮（NO）、活性氧（ROS）、IL-6、IL-1β和TNF-α的水平。肺组织的转录组学分析表明，QHG主要富集了核苷酸结合寡聚化结构域样受体（NLR）信号通路。qRT-PCR、Western blotting、免疫组织化学和免疫荧光实验证实，QHG通过NLR信号通路减轻了ALI损伤。此外，使用HPLC法确定了QHG中的七种关键成分。
我们的研究表明，QHG有效地减轻了LPS诱导的ALI，并对其作用机制和物质基础提供了初步见解。
