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目的:研究建立肝失疏泄—脂质代谢异常动物模型。方法:根据祖国医学肝失疏泄,致水谷精微失于正常输布、转化的病机特点,采用慢性应激辅助高脂饮食的复合方法,以大鼠的行为学和血脂代谢水平为观测指标,研究建立肝失疏泄—脂质代谢异常动物模型。结果:行为学观察表明,在肝失疏泄对照组,大鼠出现比较典型的肝失疏泄表现,而在复合造模组(肝失疏泄—脂质代谢异常模型组),大鼠的行为学表现则兼有肝失疏泄和高脂饮食所造成的症状特点。血脂检测结果表明,正常对照组和肝失疏泄组的血清TG、TC、HDL-C和LDL-C含量都没有显著性差异,而高脂饮食组和复合造模组的TC、HDL-C和LDL-C含量则显著高于正常对照组(P<0.05或P<0.01或P<0.001),其中复合造模组的TC、LDL-C含量和高脂饮食组相比有明显差异(P<0.05,P<0.01)。结论:应用慢性应激加高脂饮食辅助的方法,初步建立了肝失疏泄—脂质代谢异常动物模型。
Objective: To study the establishment of an animal model of hepatic dysfunction - dyslipidemia. Methods: According to the failure of the liver of Chinese medicine, the rats were induced to lose the normal transmission and transformation of Mizutani by the pathogenesis characteristics. The chronic stress-assisted high-fat diet was used as a composite method. The behavioral and lipid metabolism of rats was taken as the observation index , To study the establishment of hepatic dysfunction - animal model of abnormal lipid metabolism. Results: The behavioral observation showed that in the control group of liver failure and evacuation, the typical hepatic failure of the liver appeared. However, in the compound model group (liver dysfunction - dyslipidemia model group), rats Behavioral performance is both liver dysfunction and the symptoms caused by high fat diet caused by symptoms. The result of blood lipid test showed that there was no significant difference of TG, TC, HDL-C and LDL-C in normal control group and liver failure evacuation group, while TC and HDL-C in high-fat diet group and compound model group (P <0.05 or P <0.01 or P <0.001). The contents of TC and LDL-C in compound model group were significantly higher than those in high-fat diet group (P <0.05 or P < <0.05, P <0.01). Conclusion: Chronic stress and hyperlipidemia-assisted diet were used to establish an animal model of hepatic dysfunction and lipodystrophy.