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为了探讨异常黑胆质体液对异常黑胆质性肝癌病证模型肝硬化期的影响,在异常黑胆质载体大鼠模型的基础上,用二乙基亚硝胺(DEN)诱发建立维吾尔医异常黑胆质性肝癌病证模型大鼠发生肝硬化,对大鼠第5、7、9、11周时肝脏的外观、病理变化和超微结构进行动态观察。结果表明,模型对照组和异常黑胆质病证模型组均经过肝细胞损伤、肝细胞增生、肝硬化等改变;但异常黑胆质病证模型组大鼠肝脏外观的变化明显快于模型对照组;在同一时间,异常黑胆质病证模型组肝细胞水肿程度、不典型增生、假小叶的形成等病理表现和糖原、线粒体减少等超微结构变化均较模型对照组严重。由此可以得出,在异常黑胆质载体大鼠模型的基础上,用DEN诱导的异常黑胆质性肝癌病证模型肝脏病变的发生过程中异常黑胆质体液可能具有促进和加快肝细胞坏死,肝细胞增生灶,肝细胞增生结节,肝硬化,直至肝细胞癌过程的作用,而这一过程接近人类肝癌的发病特点和过程。表明异常黑胆质性肝癌病证模型肝硬化期的建立具有一定的可行性。
In order to investigate the effect of abnormal savda on liver cirrhosis in abnormal savda hepatocarcinoma model, based on the abnormal savda model rat model, diethylnitrosamine (DEN) was used to induce the establishment of Uighur medicine Abnormal savda hepatocarcinoma syndrome rat model of liver cirrhosis rats at the 5th, 7th, 9th and 11th weeks when the liver appearance, pathological changes and ultrastructural dynamic observation. The results showed that the model control group and the abnormal savda disease model group were all subjected to changes of hepatocyte injury, hepatocyte proliferation and cirrhosis; however, the changes of the liver appearance of the model group were significantly faster than those of the model control At the same time, the pathological changes such as hepatocyte edema, atypical hyperplasia and pseudolobule formation and ultrastructural changes of glycogen and mitochondria in model group with abnormal Savda were more serious than those in model control group. It can be drawn, based on the abnormal Savda model in rats, DEN-induced abnormal Savanna hepatocellular carcinoma syndrome model of abnormal liver tissues in the process of liver disease may have to promote and speed up the liver cells Necrosis, hepatocellular hyperplasia, hepatocellular hyperplasia nodules, liver cirrhosis, until the process of hepatocellular carcinoma, and this process is close to the incidence of human liver cancer characteristics and processes. That abnormal savda hepatobiliary disease model of liver cirrhosis of the establishment of a certain feasibility.