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目的:以小鼠肝炎病毒A59株(MHV-A59)和大肠杆菌作为生物致病因子,建立2种小鼠温病湿热证动物模型,从肝脏核因子κB(NF-κB)表达探讨温病湿热证的部分致病机制。方法:①温病湿热证的致病机制:动物随机分为正常组、模型组、肠菌组共3组,免疫组化法检测小鼠肝脏NF-κB;②造模因素在MHV-A59温病湿热证致病机制形成中的地位:动物随机分为正常组、模型组、湿热组(肥甘饮食+湿热外环境造模)、病毒组(单纯MHV-A59造模)共4组,免疫组化法检测小鼠肝脏NF-κB;③清热祛湿类方药的对温病湿热证机制的反证:动物随机分为正常组、模型组、A药组(模型组用蒿芩清胆汤治疗),B药组(模型组用黄连解毒汤治疗)、C药组(模型组用三仁汤治疗)等5组,免疫组化法检测小鼠肝脏NF-κB表达。结果:模型组、肠菌组肝脏NF-κB表达较正常组明显升高(P<0.05,P<0.01)。病毒组、模型组肝脏NF-κB表达较正常组明显升高(P<0.01),湿热组较正常组升高不明显(P>0.05),病毒组与模型组无明显差异(P>0.05)。与模型组比较,B药组肝脏NF-κB表达明显降低(P<0.05)。结论:肝脏NF-κB表达增强是温病湿热证共同的致病机制之一,在MHV-A59温病湿热证形成中,MHV-A59因素主导着炎症;清热祛湿类方药具有不同程度降低肝脏NF-κB,反证了温病湿热证的上述致病机制。
OBJECTIVE: To establish animal models of damp-heat syndrome of warm-blooded mice with mouse hepatitis A virus A59 strain (MHV-A59) and Escherichia coli as bio-pathogenic factors. To investigate the expression of nuclear factor-κB (NF- Part of the pathogenic mechanism of the card. Methods: ① Pathogenic mechanism of damp-heat Syndrome of Fever: The animals were randomly divided into normal group, model group and enterobacteriacea group. Immunohistochemistry was used to detect the expression of NF-κB in liver of mice. The pathogenesis of disease damp-heat syndrome in the formation of the position: Animals were randomly divided into normal group, model group, damp-heat group (fat diet + humid environment), the virus group (pure MHV-A59 modeling) The mice liver NF-κB was detected by the method of histochemistry; ③ The anti-heat-dampness-type prescriptions were contradictory to the damp-heat syndrome mechanism of temperature sickness: Animals were randomly divided into normal group, model group and A drug group ), Group B (model group treated with Huanglian Jiedu Decoction) and Group C (model group treated with Sanren Tang). Immunohistochemistry was used to detect the expression of NF-κB in liver of mice. Results: The expression of NF-κB in model group and enterobacteria group was significantly higher than that in normal group (P <0.05, P <0.01). Compared with normal group, the expression of NF-κB in virus and model group was significantly higher than that in normal group (P <0.01), but not in normal group (P> 0.05) . Compared with model group, the expression of NF-κB in liver of B group was significantly decreased (P <0.05). Conclusion: The increased expression of NF-κB in the liver is one of the common pathogenic mechanisms of damp-heat syndrome. In the formation of MHV-A59 damp-heat syndrome, MHV-A59 is the predominant factor of inflammation. The heat- NF-κB, reversing the above pathogenesis of warm damp-heat syndrome.