Exploring the Mechanisms of Lijin Fang on Treg/Th17 Cell Imbalance in COPD Based on Network Pharmacology.

BACKGROUND: Chronic Obstructive Pulmonary Disease (COPD) is chronic respiratory disease that severely affects patients' quality of life and is associated with high mortality rates. Investigating the imbalance between regulatory T cells (Tregs) and T helper 17 cells (Th17) in COPD treatment is crucial, as this imbalance plays a significant role in the disease's inflammatory processes. This study explores the therapeutic potential of the traditional Chinese medicine(TCM) formula, Lijin Fang (LJF), focusing on its ability to restore Treg/Th17 balance. METHODS: We employed bioinformatics and in vitro cell experiments to analyze the active components and targets of LJF. Network pharmacology, differential gene expression, pathway enrichment, ROC model prediction, and immune infiltration analyses were conducted, followed by molecular docking studies. Rat peripheral blood mononuclear cells (PBMCs) were cultured and treated with cigarette smoke extract (CSE) and LJF-containing serum, with flow cytometry, ELISA, and Western blotting used to assess relevant markers. RESULTS: Our findings demonstrate that treatment with (10% or 30%)LJF-containing serum significantly increased the proportion of Treg cells while concurrently decreasing Th17 cell populations in the 5%CSE-treated rat PBMC model (p<0.001). We observed a reduction in pro-inflammatory cytokines such as interleukin-17 (IL-17), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β), alongside an increase in the anti-inflammatory cytokine interleukin-10 (IL-10) (p<0.001). Additionally, potential therapeutic targets, including IL-10, potassium voltage-gated channel subfamily N member 4 (KCNN4), and Baculoviral IAP repeat-containing protein 3 (BIRC3), were identified. Molecular docking results indicated stable interactions between IL-10 and BIRC3 with the constituents of LJF. CONCLUSION: This study highlights LJF's anti-inflammatory potential in restoring the Treg/Th17 balance and regulating cytokine expression in COPD.