Yi-Qi-Ping-Chuan-Fang Reduces TSLP Elevation Caused by LPS + Poly(I:C) via Inhibiting TLR4/MYD88/NF- κ B Signaling Pathway.

Objective. To explore the correlation between Thymic Stromal Lymphopoietin (TSLP) and the Nuclear Factor-(NF-)kappa B signaling pathways in bronchial epithelial cells and to clarify whether the traditional Chinese medicine formula Yi-Qi-Ping-Chuan-Fang (YQPC) reduces inflammation by inhibiting TSLP/NF-kappa B signaling pathways. Methods. Cells were stimulated with LPS + Poly(I:C) and treated with YQPC. The expressions of TSLP and NF-kappa B signaling pathways related proteins P65, I kappa K, I kappa Ba, P-P65, P-I kappa K, P-I kappa Ba were detected. The effects of NF-kappa B upstreammolecules, Toll-like receptors 3 and 4, myeloid differentiation primary response gene 88 (Myd88), TIR-domain-containing adapter-inducing interferon-beta (TRIF), and downstream inflammatory cytokines, TNF-alpha, IL-1 beta, IL-6, and IL-8, were assessed. Results. The mRNA and protein expressions of TSLP were significantly increased after LPS + Poly(I:C) stimulation, the total protein I kappa Ba and I kappa K decreased (P < 0.05), and the phosphorylated protein P-P65, P-I kappa K, and P-I kappa B alpha increased. After YQPC treatment, the expression of TSLP, P-P65, P-I kappa Ba, and P-I kappa K was significantly inhibited (P < 0.05). The activation of TLR4 and MyD88 decreased, and release of IL-1 beta, IL-6, IL-8, and TNF-alpha reduced (P < 0.05). Conclusion. In summary, the expression of TSLP is activated by the NF-kappa B signaling pathway. YQPC alleviated inflammation by inhibiting TSLP through regulating the NF-kappa B activation and translocation.