Exploring the Effect and Preliminary Mechanism of Qingqi Huatan Pill on ALI Based on Network Pharmacology

DOI: 10.12201/bmr.202604.00065

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  Abstract: Objective To investigate the mechanism of Qingqi Huatan Pill in the treatment of acute lung injury (ALI) based on network pharmacology and in vitro experiments. Methods The active components and corresponding targets of Qingqi Huatan Pill were screened using the TCMSP database, and ALI-related targets were obtained from the GeneCards database. The intersecting targets were identified as potential therapeutic targets. A “Chinese medicine-component-target” network and a protein-protein interaction (PPI) network were constructed, followed by GO function and KEGG pathway enrichment analyses. An ALI model was established using LPS-induced BEAS-2B cells. Cells were divided into control group, model group, and low-, medium-, and high-dose Qingqi Huatan Pill groups. Cell viability was assessed using CCK-8 assay, TNF-α and IL-6 levels were detected by ELISA, and the protein expression of p-PI3K and p-AKT was measured by Western blot. Results A total of 92 active components and 208 corresponding targets of Qingqi Huatan Pill were identified, and 161 overlapping targets were obtained with ALI-related targets (10885). Core targets such as AKT1, IL6, and TNF were identified through PPI network analysis. KEGG enrichment analysis indicated that the PI3K-Akt signaling pathway was the primary pathway involved. In vitro experiments showed that compared with the model group, cell viability was significantly increased (P<0.05), while the levels of TNF-α and IL-6 were significantly decreased (P<0.05) in all Qingqi Huatan Pill treatment groups. Furthermore, the protein expression levels of p-PI3K and p-AKT were significantly reduced (P<0.05). Conclusion Qingqi Huatan Pill may exert protective effects against acute lung injury by inhibiting the activation of the PI3K/AKT signaling pathway and alleviating inflammatory responses.

  Key words: Qingqi Huatan Pill; acute lung injury; network pharmacology; PI3K/AKT signaling pathway

  Submit time: 9 April 2026

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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