清营解表合剂对流感病毒感染小鼠肺组织不同时相Th1/Th2细胞因子漂移的影响

目的：观察清营解表合剂对流感病毒感染小鼠Th1/Th2免疫平衡的影响。方法：以流感病毒亚洲甲型鼠肺适应株（A/PR/8/H1N1）感染小鼠为模型,采用SABC免疫组织化学法动态观察清营解表合剂干预治疗后肺部Thl型细胞因子γ-干扰素（IFN-γ）和Th2型细胞因子白介素-4（IL-4）的表达水平及IFN-γ/IL-4比值的变化。结果：感染模型组IFN-γ表达第6,9,12天较正常空白组下降。药物干预后,清营解表合剂组IFN-γ表达逐渐升高,第6,9,12天较感染模型组升高差异显著。感染模型组IL-4表达各时间点均高于正常空白组,在第6天达峰值;药物干预后,清营解表合剂组不同时间表达较感染模型组均下降,第6,9天下降显著,有统计学意义。病毒感染后,模型组较正常组IFN-γ/IL-4的比值在各时间点均降低,Th1/Th2平衡向Th2方向飘移;药物干预后,第6,9,12天清营解表合剂组较模型组IFN-γ/IL-4的比值升高有统计学意义,Thl/Th2平衡飘移得到纠正。结论：清营解表合剂可促进流感病毒感染小鼠Thl细胞因子表达,抑制Th2细胞因子的表达而提高免疫功能,调节机体的抗感染免疫平衡。

Dynamic effects of Qingying Jiebiao mixture on the shift of Th1/Th2 cytokines in the lungs of mice infected by influenza virus

Objective：To observe the effect of Qingying Jiebiao mixture（QYJBM） on immunity balance of Th1/Th2 in mice infected by influenza virus. Methods：Mice were infected by influenza virus（A/PR/8/H1N1） and treated with QYJBM,the change of Thl cytokine（IFN-γ）,Th2 eytokinc（IL-4） and the ratio of IFN-γ/IL-4 in lung tissue were dynamically observed by SABC immunohistochemistrial method. Results：After the mice were infected by influenza virus,the protein expressions of IFN-γ of the model group were lower than those of the control group on the sixth, ninth and twelfth day. The expressions of IFN-γ of QYJBM group were increased and the increase became remark- able compared with those of the model group. However,the expressions of IL-4 of the model group were higher than those of the control group,reached the peak in sixth day. The expressions of IL-4 of the treated group were remarkably decreased on different time. The ratios of IFN-γ/IL-4 of the model group were lower than those of the control group on different time. The Th1/Th2 immune balance was broken and shifted towards Th2. The ratio of IFN-γ/IL-4 of QYJBM group was increased and the increase became remarkable on the sixth,ninth and twelfth day, compared with those of the model group. The Th1/Th2 immune balance was regained. Conclusion：QYJBM can increase the immune function and adjust the immune balance of the mice infected by influenza virus by increasing the levels of IFN-γ and inhibiting the over production of IL-4.