为探讨异常黑胆质成熟剂对异常黑胆质性肝癌病证模型肝硬化期的肝脏形态学的影响,阐明异常黑胆质成熟剂在异常黑胆质性肝癌病证模型中预防肝癌的作用机理,根据维吾尔医学理论,采用多因素复制大鼠异常黑胆质性肝癌病证模型至模型大鼠发生肝硬化,并用异常黑胆质成熟剂低、中、高不同剂量(1.5,3.0,6.0g/kg)对模型全程干预,并于第7,11,15周处死大鼠,对肝脏的病理变化和超微结构进行动态观察。结果表明,低剂量组在上述时间段与病证模型组相比,病理变化和超微结构无明显改变,而中剂量组和高剂量组,与病证模型组相比,具有肝细胞结缔组织增生减少、间质炎性细胞浸润程度明显减轻、肝细胞水肿程度减轻等病理表现及肝细胞内细胞器分布不均匀、肝糖原和线粒体逐渐减少等超微结构明显变化。可以得出结论,异常黑胆质成熟剂对异常黑胆质性肝癌病证模型肝硬化期的肝脏组织形态改变有一定的保护和修复作用。

This paper discusses the effect and possible mechanism of abnormal savda munziq on the morphological structure of hepatic tissue in hepatocirrhosis phase of hepatocarcinoma carrying abnormal savda model. According to the theory of Uighur traditional medicine, multi-complicated induction methods were adopted to establish the hepatocirrhosis phase of hepatocarcinoma carrying abnormal savda disease rat model, three other drug groups were given three different dosages (1.5, 3.0, 6.0 g/kg) of abnormal savda munziq during the whole procedure, and the pathological and ultrastructural changes of the liver in the 7th, 11th, 15th weeks were observed dynamically. The result shows that at the same point in time, the pathological and ultrastructural changes of the liver in the low dose group have not been improved significantly compared with that of the abnormal savda syndrome model group, while there have been significant improvements in the middle dose group and high dose group compared with the abnormal savda syndrome model group, such as reduction of connective tissue hyperplasia, reduction of interstitial infiltration of inflammatory cells, reduction of the degree of edema of liver cells, ultrastructural changes of uneven distribution of liver intracellular organelles and gradual reduction of liver glycogen and mitochondrial. These findings indicate that abnormal savda munziq can protect and recover the morphological damage on hepatic tissue in hepatocirrhosis phase of hepatocarcinoma carrying abnormal savda model.