异常黑胆质性肝癌病证模型肝硬化期免疫、内分泌紊乱状态

 根据维吾尔医学理论，采用干寒饲养环境、干寒属性的饲料、慢性间断足底电刺激等多因素复合作用3周，建立维吾尔医异常黑胆质证载体大鼠模型后，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至模型大鼠发生肝硬化。检测外周血白细胞介素1β（IL-1β）、白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）、促肾上腺皮质激素（ACTH）、皮质醇（CORT）等免疫、内分泌指标的变化。结果表明，与正常对照组相比，异常黑胆质病证模型组血清IL-1β、IL-6和TNF-α水平显著升高（IL-1β，P<0.01；IL-6、TNF-α，P<0.001）；与模型对照组相比，异常黑胆质病证模型组IL-6和TNF-α水平显著升高（P<0.01）；与正常对照组相比，模型对照组、异常黑胆质证组、异常黑胆质病证模型组血清ACTH和CORT水平显著升高；与模型对照组相比，异常黑胆质病证模型组ACTH水平显著升高（P<0.05）。由此表明，异常黑胆质性肝癌病证模型发生肝硬化时其免疫-内分泌网络功能处于紊乱状态。在异常黑胆质性肝癌病症模型肝脏病变的发生过程中，DEN是其发生的主要原因，异常黑胆质体液起了促进作用，并且异常黑胆质体液、免疫-内分泌网络的紊乱和DEN三者之间相互联系、相互促进。

Disordered Immune-endocrin Network in Hepatocirrhosis Phase of Hepatocarcinoma of Carrying Abnormal Savda Model

According to the theory of Uighur traditional medicine, male wistar rats were fed with a diet of cold-nature under cool dry environment, stimulated with chronic and interrupted electric foot shocks to establish abnormal savda syndrome rat model in Uighur medicine in three weeks. DEN was used further to establish hepatocarcinoma carrying abnormal savda disease animal model till the hepatocirrhosis occurred. The alterations of IL-1β, IL-6, TNF-α, ACTH and CORT in serum level were monitored. The results show that compared with the normal group the serum levels of IL-1β, IL-6 and TNF-α in the abnormal savda syndrome model group were increased (for IL-1β, P<0.01; for IL-6 and TNF-α, P<0.001); compared with the model control group the serum levels of IL-6 and TNF-α in the abnormal savda syndrome model group were increased (P<0.01); compared with the normal group the serum levels of ACTH and CORT in the model control group, the abnormal savda disease group and the abnormal savda syndrome model group were all increased, with significant mathematical differences, compared with the model control group the serum level of ACTH in the abnormal savda syndrome model group was significantly increased (P<0.05). These findings indicate that the immune-endocrin network was disordered in hepatocirrhosis phase of hepatocarcinoma carrying abnormal savda model. In the process of pathological changes of hepatic tissue in hepatocarcinoma carrying abnormal savda model, DEN is the main induction agent, and abnormal savda hilit is the accelerative factor. In addition, the abnormal savda, disordered immune-endocrin network and DEN are closely related and stimulated with each other.