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目的探讨维医异常黑胆质成熟剂对多因素诱发肝癌大鼠模型的抗肝癌作用。方法将120只雄性Wistar大鼠随机分为实验组和对照组。实验组大鼠分为异黑肝癌组及异黑成熟剂高、中、低剂量组。根据维吾尔医学理论体系,实验组采用干寒饲养环境、间断足底电刺激、强迫游泳、夹尾等多因素复合作用21d建立异常黑胆质证载体大鼠模型后,在此基础上用二乙基亚硝胺(DEN)诱导20w建立异常黑胆质型肝癌病证大鼠模型,并用异常黑胆质成熟剂按高、中和低(6.0、3.0和1.5g/kg体质量)剂量全程干预,且持续进行异常黑胆质证多因素复合作用直至实验结束。对照组大鼠分为正常对照组和对照肝癌组,在正常饲养环境下未受任何刺激,21d时给予对照肝癌组饮用二乙基亚硝胺(DEN)诱导20w建立肝癌大鼠模型。20w时用免疫组织化学方法检测各组肝组织中p53和p21基因的表达水平。结果与正常对照组比较,对照肝癌组和异黑肝癌组p53和p21基因表达均明显上调(P<0.05);与对照肝癌组比较,异黑肝癌组2种基因表达也均明显上调(P<0.05);与异黑肝癌组比较,异黑肝癌3个剂量组p53和p21基因表达均明显下调(P<0.05)。结论异常黑胆质成熟剂可能通过阻遏该动物模型肝细胞中p53和p21基因的表达而起抗肝癌作用。
Objective To investigate the anti-hepatocarcinoma effect of abnormal savda of Savaria on multi-factor induced hepatocellular carcinoma rat model. Methods 120 male Wistar rats were randomly divided into experimental group and control group. Rats in the experimental group were divided into high He, medium and low dose groups of Hepatic Hepatic Carcinoma group and Hemiplegia Mature group. According to the Uyghur medical theory system, the experiment group established the rat model of abnormal savda-bearing vector on the 21st day by the combination of dry and cold feeding environment, intermittent soleus stimulation, forced swimming, Nitrosamine (DEN) induced abnormal savda hepatobaroma in rats for 20 weeks. The abnormal savda mastitis agents were used at high, medium and low doses (6.0, 3.0 and 1.5 g / kg body weight) And continued abnormal savda syndrome multi-factor combination until the end of the experiment. Rats in control group were divided into normal control group and control group. The rats in control group were not stimulated under normal feeding conditions. On the 21st day, rats in control group were given diethylnitrosamine (DEN) for 20 weeks to establish hepatoma model. Immunohistochemistry was used to detect the expression of p53 and p21 in each group at 20 weeks. Results Compared with the normal control group, the expression of p53 and p21 gene in control group and IHCC group were significantly increased (P <0.05). Compared with the control group, the expression of two genes in Hepatic Hepatic Carcinoma Group was also significantly increased (P < 0.05). Compared with the group of heterozygous hepatocellular carcinoma, the expression of p53 and p21 gene were significantly down-regulated in all the three groups (P <0.05). Conclusion Aberrant samara may play an anti-hepatocarcinoma role by blocking the expression of p53 and p21 genes in the hepatocyte of the animal model.