研究论文

异常黑胆质型肝癌病证模型肝脏形态学研究

  • 王延蛟, 哈木拉提·吾甫尔, 依马木·买买提依明, 热斯拉特·艾力木, 阿尤甫江·阿布都热依木, 斯坎德尔·白克力
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  • 1. 新疆医科大学基础医学院, 乌鲁木齐 830011;
    2. 新疆医科大学药学院, 乌鲁木齐 830011
王延蛟,副教授,研究方向为维医异常黑胆质型肝癌发病的分子机制,电子信箱:dss-02458@163.com

收稿日期: 2013-12-16

  修回日期: 2014-04-09

  网络出版日期: 2014-05-29

基金资助

国家自然科学基金项目(81160545)

A Rat Model of Hepatocarcinoma Carrying Abnormal Savda and Its Morphological Study

  • WANG Yanjiao, UPUR Halmurat, MAMATIMIN Imam, HELIM Resalat, ABDURIYIM Ayupjan, BAKRI Iskandar
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  • 1. College of Basic Medicine, Xinjiang Medical University, Urumqi 830011, China;
    2. College of Pharmacy, Xinjiang Medical University, Urumqi 830011, China

Received date: 2013-12-16

  Revised date: 2014-04-09

  Online published: 2014-05-29

摘要

为探讨异常黑胆质体液对异常黑胆质型肝癌病证模型的影响,在异常黑胆质载体大鼠模型基础上用二乙基亚硝胺(DEN)诱导建立维吾尔医异常黑胆质型肝癌病证模型大鼠,并对大鼠第11、15、20 周时肝脏的外观、病理变化等进行动态观察。20 周后,异常黑胆质病证模型组和模型对照组均发生癌变,前者成癌率(100%)明显高于后者(72%)(P<0.01)。总之,在异常黑胆质载体大鼠模型的基础上,用DEN 诱导的异常黑胆质型肝癌病证模型肝癌的发生过程中,异常黑胆质体液具有促进和加快肝脏病变的作用。本研究成功建立了异常黑胆质并DEN 诱导的肝癌病证大鼠模型。

本文引用格式

王延蛟, 哈木拉提·吾甫尔, 依马木·买买提依明, 热斯拉特·艾力木, 阿尤甫江·阿布都热依木, 斯坎德尔·白克力 . 异常黑胆质型肝癌病证模型肝脏形态学研究[J]. 科技导报, 2014 , 32(14) : 74 -78 . DOI: 10.3981/j.issn.1000-7857.2014.14.012

Abstract

The effect of abnormal savda on the initiation and development of hepatocarcinoma was studied by establishing a rat model of hepatocarcinoma carrying abnormal savda. A rat model with abnormal savda disease was first established, and diethylnirtosamine (DEN) was used to further establish a model of hepatocarcinoma carrying abnormal savda under Uighur medicine treatment. The morphology and pathological changes of the liver were observed at the 11th, 15th and 20th week. After the 20th week, cancerization was induced both in the experimental group (hepatocarcinoma with abnormal savda) and the model control group (without abnormal savda syndrome but DEN treatment), but the pathological changes of the liver surface in the experimental group appeared faster than those in the model control group, and the incidence of hepatocellular carcinoma (100%) of the former was significantly higher than that of the latter (72%) (P<0.01). These findings indicate that abnormal savda hilit facilitates transformation of hepatocyte to hepatocellular carcinoma.

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