中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (37): 6883-6886.doi: 10.3969/j.issn.1673-8225.2011.37.011

• 组织构建实验造模 experimental modeling in tissue construction • 上一篇    下一篇

急性肝功能衰竭模型大鼠缝隙连接蛋白的表达

王开阳1，肖樟生2，蒋星星2，傅华群2   

  1. 南昌大学第二附属医院，1急诊科，2肝胆外科，江西省南昌市  330006
  • 收稿日期:2011-03-01 修回日期:2011-04-10 出版日期:2011-09-10 发布日期:2011-09-10
  • 通讯作者: 傅华群，硕士，主任医师、教授，南昌大学第二附属医院肝胆外科，江西省南昌市 330006 ncdxfhq@yahoo.com.cn
  • 作者简介:王开阳★，男，1852年生，江西省南昌市人，汉族，硕士，医师，主要从事肝胆外科基础与临床研究。 kaiyang3937@ 126.com
  • 基金资助:

    江西省教育厅资助项目(GJJ09105)。

Connexin expression in a rat model of acute liver failure

Wang Kai-yang1, Xiao Zhang-sheng2, Jiang Xing-xing2, Fu Hua-qun2   

  1. 1Department of Emergency, 2Department of Hepatobiliary Surgery, Second Affiliated Hospital of Nanchang University, Nanchang   330006, Jiangxi Province, China
  • Received:2011-03-01 Revised:2011-04-10 Online:2011-09-10 Published:2011-09-10
  • Contact: Fu Hua-qun, Master, Chief physician, Professor, Department of Hepatobiliary Surgery, Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China ncdxfhq@yahoo. com.cn
  • About author:Wang Kai-yang★, Master, Physician, Department of Emergency, Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi Province, China kaiyang3937@126. com
  • Supported by:

    a grant from Education Department of Jiangxi Province, No. GJJ09105*

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被引次数

1

摘要：

背景：缝隙连接蛋白是组成相邻细胞间通道的主要结构，承担着细胞间的多种物质传输和信息交流的作用，可协助调节细胞的生长和分化。
目的：观察急性肝功能衰竭大鼠缝隙连接蛋白32表达与肝细胞增生的关系。
方法：采用乳果糖+庆大霉素灌胃和四氯化碳+橄榄油腹腔注射法建立大鼠急性肝功能衰竭模型。造模前7 d，苯巴比妥组大鼠用含体积分数0.08%苯巴比妥的水喂养，直至取材。对照组大鼠不造模，仅腹腔注射橄榄油与生理盐水的混合物。分别于造模后1，3，7，10，14 d取材。
结果与结论：大鼠肝功能衰竭后，部分大鼠出现死亡，存活大鼠肝细胞出现变性坏死，谷丙转氨酶明显升高，肝细胞间缝隙连接蛋白32 mRNA及蛋白表达明显降低。苯巴比妥可降低肝功能衰竭大鼠的死亡率，同时在一定程度上降低肝功能衰竭大鼠谷丙转氨酶水平及肝细胞间缝隙连接蛋白32 mRNA及蛋白的表达。说明通过苯巴比妥预先下调肝细胞间的缝隙连接蛋白32水平可以减轻急性肝功能衰竭大鼠急性期的肝脏损害，促进残存肝细胞增生和肝功能的好转，降低急性肝功能衰竭大鼠的病死率。

关键词: 缝隙连接蛋白32, 急性肝功能衰竭, 肝细胞, 增生, 大鼠, 组织工程

Abstract:

BACKGROUND: Connexin is the primary structure to compose intracellular channel, is responsible for substance transport and information exchange and can help regulate cell growth and differentiation.
OBJECTIVE: To investigate the relationship of connexin 32 expression and hepatocyte proliferation in a rat model of acute liver failure.
METHODS: Rat models of acute liver failure were established by intragastric administration of lactulose and gentamicin and intraperitoneal administration of carbon tetrachloride and olive oil. From 7 days before acute liver failure induction, phenobarbital group rats were raised with water containing 0.08% phenobarbital till sample harvesting. Acute liver failure was not induced in the control group, and only intraperitoneal administration of mixture of olive oil and physiological saline was performed. At 1, 3, 7, 10, and 14 days after modeling, samples were harvested.
RESULTS AND CONCLUSION: After liver failure, some rats died, the hepatocytes of surviving rats were degenerative and necrotic, glutamic-pyruvic transaminase was obviously increased, connexin 32 mRNA and protein expression was obviously decreased. Phenobarbital can decrease the mortality of rats with liver failure and it can also decrease glutamic-pyruvic transaminase level and connexin 32 mRNA and protein expression. These results showed that phenobarbital can downregulate connexin 32 expression in the hepatocytes, which can alleviate the liver damage of liver failure rats during the acute stage, promote the proliferation of remaining hepatocytes, improve liver function, and finally decrease the mortality of rats with acute liver failure.

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