[1]林立腾,蔡明岳,黄文薮,等.门静脉高压症小鼠模型构建 [J].介入放射学杂志,2018,27(03):242-246.
 LIN Liteng,CAI Mingyue,HUANG Wensou,et al.The establishment of portal hypertension model in mice[J].journal interventional radiology,2018,27(03):242-246.
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门静脉高压症小鼠模型构建 



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《介入放射学杂志》[ISSN:1008-794X/CN:31-1796/R]

卷:
27
期数:
2018年03期
页码:
242-246
栏目:
实验研究
出版日期:
2018-03-25

文章信息/Info

Title:
The establishment of portal hypertension model in mice
作者:
林立腾 蔡明岳 黄文薮 黄敬君 兰 天 朱康顺
Author(s):
LIN Liteng CAI Mingyue HUANG Wensou HUANG Jingjun LAN Tian ZHU Kangshun
Department of Minimally- Invasive Interventional Radiology, Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province 510260, China
关键词:
【关键词】 门静脉高压症 胆管结扎 四氯化碳 小鼠模型
文献标志码:
A
摘要:
【摘要】 目的 构建小鼠胆总管结扎(BDL)及四氯化碳(CCl4)诱导的两种门静脉高压症(PHT)模型。方法 24只C57BL/6小鼠,随机分成4组(BDL组及相应对照组,CCl4诱导组及相应对照组),每组6只。BDL及CCl4诱导法构建PHT小鼠模型后,经门静脉主干穿刺测取门静脉压,并通过血清谷氨酸转氨酶(ALT)及天冬氨酸转氨酶(AST)水平检测,肝脏切片苏木精-伊红(HE)及天狼星红染色,α- 平滑肌肌动蛋白(SMA)免疫组化检查分别对模型肝功能、肝纤维化及肝星状细胞激活情况进行评价。结果 两种建模方法均使小鼠门静脉压上升,CCl4诱导组上升更为显著。两模型组小鼠与相应对照组相比,均呈现严重肝功能损伤、肝纤维化及肝星状细胞激活。结论 BDL及CCl4诱导方法均能成功构建PHT小鼠模型,其门静脉压、血清学生化指标及肝脏病理学改变均符合PHT特点。

参考文献/References:

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备注/Memo

备注/Memo:
(收稿日期:2017-04-12)
(本文编辑:边 佶)
更新日期/Last Update: 2018-03-19