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目的:动态观察板蓝根对流感病毒感染所致小鼠炎性因子的变化及对气管、肺组织病理损伤的影响。方法:建立流感病毒肺适应株(FM1)感染的肺炎小鼠模型,在FM1株感染1、3、5、7d,采用免疫组化方法观察空白对照组、模型组和板蓝根组小鼠肺组织中TNF-α、IL-6、和IFN-γ抗原分布。并在光学显微镜和气管扫描电镜下观察各组动物肺组织病变情况。结果:FM1感染后第3、5天小鼠肺组织中TNF-α、IL-6和IFN-γ明显增加(P<0.01,P<0.05),用板蓝根干预后第3、5天小鼠肺组织中TNF-α、IL-6较模型组有所降低(P<0.05),而IFN-γ较模型组有所升高(P<0.05)。通过光镜下和气管扫描电镜观察板蓝根组在感染后气管、肺组织病变程度较模型组明显减轻。结论:板蓝根能够显著改善FM1株感染所致炎性反应,并可修复气管、肺组织的病理损伤。
OBJECTIVE: To observe the changes of inflammatory cytokines and the pathological changes of trachea and lung in mice induced by influenza virus. Methods: The pneumonia model of mice infected with influenza virus lung-adapted strain (FM1) was established. The FM1 strain was infected at 1, 3, 5, and 7 days after infection. Immunohistochemical method was used to observe the expression of IL- TNF-α, IL-6, and IFN-γ antigen distribution. The pathological changes of lung tissue in each group were observed under optical microscope and tracheal scanning electron microscope. Results: The levels of TNF-α, IL-6 and IFN-γ in the lungs of FM1 infected mice were significantly increased (P <0.01, P <0.05) on the 3rd and 5th day after FM1 infection. Compared with the model group, the levels of TNF-α and IL-6 in the model group decreased (P <0.05), while the level of IFN-γ in model group increased (P <0.05). By light microscopy and tracheal scanning electron microscopy Radix isatidis in the trachea, lung tissue lesions significantly reduced compared with the model group. Conclusion: Radix isatidis can significantly improve the inflammatory response induced by FM1 infection, and can repair the pathological injury of trachea and lung tissue.