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目的:以MHV-A59和大肠杆菌作为生物致病因子,建立两种小鼠温病湿热证动物模型,从Th1/Th2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3组:正常组、模型组、肠菌组,ELISA法检测小鼠血清IL-4、IFN-γ水平;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4组: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),ELISA法检测小鼠血清IL-4、IFN-γ水平;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5组: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),ELISA法检测小鼠血清IL-4、IFN-γ水平。结果:①模型组、肠菌组血清Th1/Th2(IFN-γ/IL-4)比值较正常组明显升高(P<0.05或P<0.01)。②病毒因素主要影响到IFN-γ水平,致使模型组Th1/Th2比值较正常组明显升高(P<0.05)。③与模型组比较,A药组Th1/Th2比值明显趋于平衡(P<0.05)。结论:Th1/Th2失衡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T细胞免疫紊乱,清热祛湿类方药具有不同程度改善Th1/Th2失衡的作用,反证了温病湿热证的上述致病机制。
OBJECTIVE: To establish two animal models of damp-heat syndrome of fever in mice by using MHV-A59 and Escherichia coli as bio-pathogenic factors, and to explore some pathogenic mechanisms of damp-heat syndrome of warm-disease from Th1 / Th2. Methods: ① Pathogenic mechanism of damp-heat Syndrome of Fever: The animals were randomly divided into 3 groups: normal group, model group, enterobacteriaceae group and ELISA method to detect serum IL-4 and IFN-γ levels; -A59 temperature and damp-heat syndrome pathogenesis formation status: Animals were randomly divided into 4 groups: normal group, model group, damp-heat group (Feigan diet + humid environment), the virus group (pure MHV-A59 modeling ), Serum IL-4, IFN-γlevel of mice were detected by ELISA; ③ Antipyretics of dampness and dampness prescriptions on damp-heat syndrome mechanism of temperature sickness: Animals were randomly divided into 5 groups: normal group, model group, The model group was treated with Qinglian Qingdan Decoction), B group (model group treated with Huanglian Jiedu Decoction), C group (model group treated with Sanren Decoction), the serum IL-4, IFN-γ Level. Results: ① The levels of Th1 / Th2 (IFN-γ / IL-4) in model group and enterobacteriaceae group were significantly higher than those in normal group (P <0.05 or P <0.01). ② The viral factors mainly affected the level of IFN-γ, which led to a significant increase of Th1 / Th2 ratio in model group compared with normal group (P <0.05). ③ Compared with model group, the ratio of Th1 / Th2 in group A obviously got balance (P <0.05). Conclusion: The imbalance of Th1 / Th2 is one of the common pathogenic mechanisms of damp-heat syndrome. In the formation of MHV-A59 damp-heat syndrome, MHV-A59 predominantly leads to T cell immune disorder. / Th2 imbalance of the role, evidence of the damp-heat syndrome of the pathogenic mechanism.