论文部分内容阅读
目的:观察升降散对亚甲型流感病毒鼠肺适应株FM1感染小鼠肺组织细胞间黏附分子-1(ICAM-1)和核转录因子κB p65(NF-κB p65)表达的影响,探讨升降散抑制肺损伤的作用及配伍机制。方法:建立亚甲型流感病毒鼠肺适应株FM1感染小鼠肺炎模型,分别用二步法免疫组化、Western blot、RT-q PCR检测升降散全方、升降散拆方、升降散与麻杏甘石汤合方对小鼠肺组织ICAM-1、NF-κBp65蛋白及mRNA表达的影响。结果:三种检测方法结果基本一致,病毒性肺炎小鼠肺组织ICAM-1、NF-κBp65蛋白及mRNA表达增强,升降散全方(4.55g/kg)可以显著降低其表达,作用明显优于拆方组,同时也一定程度提升了麻杏甘石汤(5.46g/kg)组的抑制作用。结论:升降散全方开上与泄下协同配伍,能显著抑制病毒性肺炎小鼠肺组织ICAM-1、NF-κBp65的过度表达而减轻肺损伤,可以作为治疗病毒性肺炎的基本配伍用方。
Objective: To observe the effects of Shengjiang San on the expression of intercellular adhesion molecule-1 (ICAM-1) and NF-κB p65 in the lung of FM1-infected mice induced by FMDV, Scattering lung injury and the mechanism of compatibility. Methods: A pneumonia model was established in FM1 mice infected with influenza A virus. The two groups were immunostained with two-step immunohistochemical method. Western blot and RT-q PCR were used to detect the effect of Shengjiang Powder, Effects of Gan Xing Shi Decoction on Protein and mRNA Expression of ICAM-1 and NF-κBp65 in Lung Tissue of Mice. Results: The results of the three methods were basically the same. The expressions of ICAM-1 and NF-κBp65 in lungs of mice with viral pneumonia were significantly increased, and the expression of ICAM-1 and NF-κBp65 in lungs of mice with viral pneumonia was significantly decreased Demolition of the square group, but also to some extent enhance the Maxing Gan Shi Tang (5.46g / kg) group inhibition. Conclusion: Ascending and descending all-round opening and discharge of synergistic compatibility, can significantly inhibit viral pneumonia in mice lung tissue ICAM-1, NF-κBp65 overexpression and reduce lung injury, can be used as the basic compatibility of treatment of viral pneumonia .