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Juan LI, Meiling WANG, Lihong LIU. Effect of Xiyanping on Inflammatory Microenvironment of COPD Model Based on TLR3-MAPK Signaling Pathway[J]. Journal of Kunming Medical University.
Citation: Juan LI, Meiling WANG, Lihong LIU. Effect of Xiyanping on Inflammatory Microenvironment of COPD Model Based on TLR3-MAPK Signaling Pathway[J]. Journal of Kunming Medical University.

Effect of Xiyanping on Inflammatory Microenvironment of COPD Model Based on TLR3-MAPK Signaling Pathway

  • Received Date: 2025-06-25
  •   Objective  Based on Toll-like receptor 3 protein (TLR3)- mitogen-activated protein kinase (MAPK) signaling pathway, the effect of Xiyanping on inflammatory microenvironment of chronic obstructive pulmonary disease (COPD) model was discussed.   Methods  A mouse model of COPD induced by Cigarette Smoke (CS) was established and treated with XYP (low, medium and high). Human Bronchial Epithelial cells (HBE) were exposed to Cigarette Smoke Extract (CSE) and treated with XYP or TLR3 agonist poly(I:C). The expression of α-Smooth Muscle Actin (α-SMA), Collagen type I (Collagen I), TLR3 and MAPK signaling pathway proteins were detected by western blot.   Results  Compared with the Ctrl group, the score of HE staining in CS group increased (P < 0.05). Compared with CS group, the score of HE staining in XYP-H group decreased (P < 0.05). Compared with the Ctrl group, the levels of CollagenⅠ, α-SMA, TLR3 and MAPK signaling pathway protein in lung tissue of CS group increased (P < 0.05). Compared with CS group, the expression of CollagenⅠ, α-SMA, TLR3 and MAPK protein in XYP-H group decreased (P < 0.05). In vitro experiment, compared with CSE group, the expression of CollagenⅠ, α-SMA, TLR3 protein and MAPK signaling pathway protein in HBE cells in CSE+XYP-H group decreased (P < 0.05). Compared with CSE+XYP-H group, the expression levels of CollagenⅠ and α-SMA in CSE+XYP-H+poly(I:C) group increased (P < 0.05).   Conclusion  Xiyanping injection can alleviate the development of pulmonary fibrosis in the process of COPD, and its mechanism may be related to inhibiting the activation of TLR3-MAPK signaling pathway.
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