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

Background and Purpose 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 inflammation-related 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.