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目的:用疏肝健脾法方药干预、反证鸭乙型肝炎病毒(DHBV)感染肝郁脾虚证动物模型的效果。方法:将90只1日龄雏鸭随机分为病毒组、模型组、病毒干预组、模型干预组各15只,限制组、限制干预组和空白组各10只,共7组。病毒组、模型组、病毒干预组、模型干预组通过腹腔注射DHBV-DNA强阳性血清,或限制或强行活动造出满足要求之相应各组,比较各组雏鸭不同时间DHBV-DNA拷贝数对数值变化、啄癖率、进食时间及强行下水时间,并进行肝脏病理学检查。结果:第7天(T7)各攻毒组DHBV-DNA拷贝数对数值比较,差异无显著性意义(P>0.05),第28天(T28)病毒组、模型组DHBV-DNA拷贝数对数值均明显高于病毒干预组、模型干预组,差异均有显著性意义(P<0.05)。模型组和限制组发生啄癖的雏鸭数明显多于其余各组,模型组、限制组的啄癖率与空白组比较,差异均有非常显著性意义(P<0.01)。T28模型组、限制组的进食时间、强行下水时间均明显较其余各组短,与空白组比较,差异均有非常显著性意义(P<0.01);病毒组与空白组比较,差异也有显著性意义(P<0.05);各干预组与空白组比较,差异亦均有显著性意义(P<0.05);各干预组与病毒组比较,差异均有显著性意义(P<0.05)。除空白组外,其余各组肝细胞均见有轻度变性,肝细胞内见脂肪变性和透明样变性。模型组、病毒组有点灶状或虫蛀状肝细胞坏死;门管区均见炎症细胞浸润,主要为淋巴细胞、少量组织细胞,偶见浆细胞;肝实质组织有不同程度的淋巴细胞浸润,胆管轻度增生,肝窦轻度扩张。结论:慢性乙型肝炎肝郁脾虚证的临床表现可以部分通过雏鸭模型再现和模拟,从而表现出相关症状和体征,成为中西医结合的病证动物模型。
OBJECTIVE: To observe the effect of the method of dissolving liver and invigorating the spleen prescription on the animal model of liver qi stagnation and spleen deficiency syndrome induced by duck hepatitis B virus (DHBV). METHODS: Ninety ducklings were randomly divided into virus group, model group, virus intervention group, and model intervention group each with 15 animals. There were 10 groups in the restriction group, restricted intervention group, and blank group, 7 groups in total. Viral group, model group, virus intervention group and model intervention group were injected intraperitoneally with strong positive serum of DHBV-DNA, or restricted or forced activity to create the corresponding groups to meet the requirements, and the DHBV-DNA copy number of each group of ducklings was compared at different times. Numerical changes, delirium rates, eating times, and forced watering times, and liver pathology were performed. RESULTS: There was no significant difference in the DHBV-DNA copy number of each challenge group on the 7th day (T7) (P>0.05). On the 28th day (T28), the DHBV-DNA copy number of the virus and model groups was logarithmically Both were significantly higher than the virus intervention group and the model intervention group, with significant differences (P<0.05). The number of ducklings in the model group and the restricted group was significantly higher than that in the remaining groups. The difference between the model group and the restricted group compared with the blank group was significant (P<0.01). The feeding time and forced watering time of the T28 model group and the restricted group were significantly shorter than those of the other groups. Compared with the blank group, the difference was significant (P<0.01); the difference between the virus group and the blank group was also significant. Significance (P<0.05); The difference between the intervention group and the blank group was also significant (P<0.05); there was a significant difference between the intervention group and the virus group (P<0.05). Except for the blank group, all other groups showed slight degeneration of liver cells, and there was fatty degeneration and hyaline degeneration in the liver cells. The model group and the virus group had a spotty or necrotic hepatocyte necrosis; inflammatory cells infiltrated in the portal area, mainly lymphocytes, a small amount of tissue cells, occasionally plasma cells; liver parenchyma with varying degrees of lymphocyte infiltration, bile duct Mild hyperplasia, mild sinusoidal expansion. Conclusion: The clinical manifestation of chronic hepatitis B with liver depression and spleen deficiency syndrome can be partially reproduced and simulated by the duckling model, which shows the related symptoms and signs, and has become an animal model of integrated traditional Chinese and western medicine.