Mechanism of Platycodonis radix in Inhibiting Epithelial-Mesenchymal Transition in Mycoplasma Pneumoniae
Objective:To investigate the therapeutic effect of Platycodonis radix on mycoplasma pneumoniae infection in Beas-2B cells and mice.Methods:Beas-2B cells were divided into groups,and a mycoplasma pneumonia model was established,with drug administration for 1 day.HE staining was used to observe the cell growth status in each group,and MTT and CCK-8 assays were used to assess cell viability.Sixty BALB/c mice were randomly divided into six groups:blank group,model group,azithromycin group,high-dose,medium-dose,and low-dose Platycodonis radix groups,with 10 mice per group.A Mycoplasma pneumonia model was established in mice using the nasal drop method.Lung pathology was observed using HE staining,and the expression levels of AQP1,Wnt-5α,and β-catenin were detected by immunohistochemistry and RT-PCR.Elisa was used to measure serum SOD,TNF-α,and IL-6 levels.RT-PCR was used to detect the effect of AQP1 inhibitor on the mRNA expression of AQP1,Wnt-5α,and β-catenin in Beas-2B cells.Results:In the model group,Beas-2B cells lost their original morphology and decreased in number.The protein and mRNA expression levels of AQP1 in mouse lung tissues were reduced(P<0.05,P<0.01),while the protein and mRNA levels of Wnt-5α and β-catenin were increased(P<0.05,P<0.01).Serum SOD levels decreased,and serum TNF-α and IL-6 levels increased(P<0.05,P<0.01).Compared with the model group,Platycodonis radix significantly improved the growth state of Beas-2B cells.The expression of AQP1 protein and mRNA in mouse lung tissues increased(P<0.05,P<0.01),while Wnt-5α and β-catenin protein and mRNA levels decreased(P<0.05,P<0.01).Serum SOD levels increased,and TNF-α levels decreased(P<0.05,P<0.01).Compared with the blank group,AQP1 inhibitors suppressed AQP1 mRNA expression in Beas-2B cells(P<0.05,P<0.01),leading to the upregulation of Wnt-5α and β-catenin mRNA expression(P<0.05,P<0.01).Conclusion:Platycodonis radix inhibits epithelial-mesenchymal transition in lung tissues caused by Mycoplasma pneumoniae by regulating AQP1 expression through the Wnt/β-catenin signaling pathway,thus protecting lung tissues.