清热祛湿法抗流感病毒的实验研究

目的 观察清热祛湿法对流感病毒所致小鼠病毒性肺炎的作用,通过探讨清热祛湿药物的抗流感病毒免疫调节机制,为指导临床辨证治疗流感提供实验依据.方法 （1）观察清热祛湿法体外抗病毒作用及对小鼠流感病毒性肺炎的影响.（2） 用FM1株甲1型流感病毒感染小鼠.制作病毒性肺炎模型,将小鼠随机分为正常组、模型组、蒿芩清胆汤组、病毒唑对照组,分别用单标法流式细胞仪及ELISA法测定四组小鼠外周血T淋巴细胞哑群（（CD3/CD4、CD8）百分比及比值及血清IL-4、IL-18、IFN-γ的含量.结果 清热祛湿法在体外对流感病毒FM1株无明显的抑制作用,但对小鼠流感病毒性肺炎均有抑制作用,与模型对照组比较,差异有显著性意义（P〈0.05）,与病毒唑组比较,差异无显著性意义（P〉005）蒿芩清胆汤对小鼠感染流感病毒FM1后血中的CD3＋CD4＋百分比和CD3＋CD4＋/CD3＋CD8＋比值下降有一定的抑制作用并且能够降低模型小鼠血清TIL-18及IFN-r的值.结论 清热祛湿药物对流感病毒具有抑制作用,但不是直接杀死流感病毒,而是一方面通过调整T细胞亚群的百分率或CD4＋CD4＋/CD4＋CD8＋比值,另一方面通过降低IFN-r、IL-18表达水平,对流感病毒感染引起的细胞免疫功能降低有一定的抑制作用,从而减少异常的细胞免疫反应,调节和加强体液免疫功能,有利于损伤组织的修复.

Eliminating heat and wetness evil therapy for influenza virus infection

Objective To observe the role of eliminating heat and wetness evil in mice with viral pneumonia due to influenza virus infection, and to provide experimental support for clinical differentiation and treatment by exploring the immune regulating mechanism of this traditional Chinese therapy for influenza virus. Methods The antiviral effect of the therapy was observed in vitro, so was the role of this treatment in pneumonia due to influenza virus infection in mice. The rat model of viral pneumonia was established by using FM1 strains. The mice were randomly assigned to normal group, model group, Haoqinqingdan decoction group, or ribavirin group. The rates of CD3/CD4 and CD8 were detected by flow cytometry, so were serum levels of IL-4, IL-8, and IFN-γ by ELISA. Results The therapy did not have an inhibiting effect on FM1 strains, but did have on influenza virus-induced pneumonia; there was a significant difference as compared with the model group (P<0.05); but there was no significant difference as compared with the ribavirin group (P>0.05). Haoqinqingdan decoction had some inhibiting effect on the decreases in the rates of CD3+CD4+ and CD3+CD4+/CD3+CD8+ and reduced levels of TIL-18 and IFN-γ. Conclusions Eliminating heat and wetness evil therapy can not kill influenza virus directly. It reduces abnormal cellular immune response and strengthen humoral immune function which is beneficial of the repair of damaged tissues by adjusting the rate of CD3+CD4+/CD3+CD8+ and by reducing the expression levels of IFN-γ and IL-18.