Effect of Qibai Pingfei Capsules on the HMGB1/TLR4/NF-κB Signaling Axis in CSE-induced Inflammation of 16HBE Cells

Background and Objectives: Chronic inflammation resulting from cigarette smoke extract (CSE) is frequently driven by activation of the high mobility group box 1 (HMGB1)–toll-like receptor 4 (TLR4)–nuclear factor kappa B (NF-κB) signaling cascade. This study was designed to explore the regulatory influence of Qibai Pingfei Capsules (QBPF) on inflammationrelated pathways in 16HBE cells, a human bronchial epithelial cell line, following CSE treatment. We also assessed the impact of QBPF on NF-κB signaling dynamics and cytokine production using a co-culture model with THP-1-derived macrophages. Materials and Methods: Levels of inflammatory mediators were quantified via enzyme-linked immunosorbent assay and quantitative reverse transcription polymerase chain reaction, while protein expression and intracellular localization were analyzed through Western blotting and immunofluorescence. NF-κB activity was further verified by RNA interference and overexpression techniques. Results: QBPF markedly mitigated the inflammatory responses induced by CSE, as evidenced by decreased cytokine output and reduced transcription of HMGB1, toll-like receptor 2, TLR4, and myeloid differentiation primary response gene 88. Furthermore, QBPF hindered the nuclear translocation of NF-κB and disrupted upstream molecular events linked to its activation. Conclusion: QBPF demonstrates potent anti-inflammatory potential through modulation of NF-κB-associated signaling networks. The current findings emphasize QBPF’s value as a prospective therapeutic candidate for controlling smoke-induced airway inflammation and suggest its broader applicability to respiratory disorders characterized by chronic inflammation.