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Pingchuan formula(平喘方) improves allergic asthma in mice through inhibiting nuclear factor-kappa B/mitogen-activated protein kinase signaling pathway

WU Mingyun  YU Jianer  BAI Li  XUE Zheng  JIANG Shenhua  LI Liqing  PIAO Xiang  XU Wanchao  WANG Jiani  SHEN Qian  
【摘要】:OBJECTIVE:To examine the role and decipher the mechanism of Pingchuan formula(平喘方, PCF) in treating allergic asthma.METHODS:The mice were treated with saline,dexamethasone(DXM) and PCF for 1 week after the asthma model was established and their respiratory function including respiratory resistance(RI),pulmonary dynamic compliance(Cdyn) and maximum voluntary ventilation(MVV) were measured.In addition, cellular changes in bronchoalveolar lavage fluid(BALF) and pathological changes in lung biopsy as well as the expression level ofα-smooth muscle actin(α-SMA), transforming growth factor-beta1(TGF-β1) in BALF and interleukin-5(IL-5),interleukin-13(IL-13), tumor necrosis factor-α(TNF-α), interferon-γ(IFN-γ), nuclear factor-kappa B-p65(NF-κBp65), inhibitor-α of nuclear transcription factor κB(IκBα), p38 mitogen-activated protein kinase(p38 MAPK), c-jun n-terminal kinase(JNK) and its phosphorylated proteins in lung tissue were also examined and compared among different groups.RESULTS:Our data suggested that the respiratory functions were significantly improved and the pathological changes ameliorated in the DXM group and the PCF group compared to the model group.Both DXM and PCF effectively decreased the number of eosinophils, lymphocytes, and neutrophils in BAL as well as the secretion ofα-SMA and TGF-β1,IL-5, IL-13, while increased the expression of TNF-αand IFN-γ. Furthermore, our study indicated that the NF-κBp65, IκBα, p38 MAPK and JNK pathways were inhibited under the treatment of PCF.CONCLUSION:Our data indicated that PCF can attenuate the inflammatory response in asthma through inhibiting the NF-κB/MAPK signaling pathway. This study not only supported the use of PCF in allergic asthma in clinic but also shed light upon afurtherunderstandingofthediseasepathogenesis.

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