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Na~+-牛磺酸转运体基因在急性肝内胆汁淤积大鼠肝组织的表达及意义
引用本文:张丽娟,黄方,黄志华.Na~+-牛磺酸转运体基因在急性肝内胆汁淤积大鼠肝组织的表达及意义[J].临床儿科杂志,2009,27(10).
作者姓名:张丽娟  黄方  黄志华
作者单位:1. 华中科技大学同济医学院附属同济医院儿科,湖北武汉,430030
2. 襄樊市中心医院儿科,湖北襄樊,441000
摘    要:目的 通过研究α-异硫氰酸萘酯(ANIT)所致的急性肝内胆汁淤积大鼠肝组织Na+-牛磺酸转运体基因(ntcp)表达的变化,以进一步探讨急性肝内胆汁淤积发生的分子机制.方法 选用40只幼年雄性SD大鼠为实验对象,随机分为正常对照组(8只)、中毒组(32只).中毒组幼鼠按100 mg/kg一次性灌服ANIT诱导急性肝内胆汁淤积病变.观察各组在灌服ANIT后24、48、72和96 h血清总胆红素(TB)、丙氨酸转氨酶(ALT)的浓度,同时用RT-PCR测定肝组织中ntcp-mRNA的表达,并在光学显微镜下观察肝脏的形态学改变.实验结果采用SPSS软件包分析.结果 灌服ANIT后,中毒组大鼠血清ALT、TB逐渐升高,24 h增加明显,48 h达高峰,72 h逐渐下降,96 h已显著下降,差异有统计学意义(P<0.05).中毒组大鼠肝组织ntcp-mRNA表达水平低于正常对照组,48 h表达最低,72 h逐渐恢复.差异有统计学意义(P<0.05).结论 ANIT所致的急性肝内胆汁淤积使肝脏功能受损,导致血清酶学改变.急性胆汁淤积肝组织基底膜ntcp基因转录水平明显下降为机体的一种负反馈机制,可减轻胆汁淤积程度,保护肝细胞.

关 键 词:Na+-牛磺酸转运体  肝内胆汁淤积  逆转录多聚酶链反应  α-异硫氰酸萘酯

Expression of Na~+-taurocholate co-transporting peptide in liver of rats with acute intrahepatic cholestatic hepatic injury
ZHANG Li-juan,HUANG Fang,HUANG Zhi-hua.Expression of Na~+-taurocholate co-transporting peptide in liver of rats with acute intrahepatic cholestatic hepatic injury[J].The Journal of Clinical Pediatrics,2009,27(10).
Authors:ZHANG Li-juan  HUANG Fang  HUANG Zhi-hua
Institution:1.Department of Pediatrics;Tongji Hospital Affiliated to Tongji Medical College;Huazhong University of Science and Technology;Wuhan 430030;Hubei;China;2.Department of Pediatrics;Xiangfan Centre Hospital;Xiangfan 441000;China
Abstract:Objective To investigate the gene expression of Na+-taurocholate co-transporting peptide (ntcp) in liver of rats with acute intrahepatic cholestatic hepatic injury induced by alpha-naphthylisothiocyanate ( ANIT) . Methods Forty young male SD rats were randomly assigned into control group (8) and intoxication group (32). A single dose (100 mg/kg) of ANIT was administered by gavage to each rat in intoxication group to induce intrahepatic cholestasis. The specimens of hepatic tissue and serum were collected at...
Keywords:Na+-taurocholate co-transporting polypeptide  intrahepatic cholestas  RT-PCR  alphana- phthylisothiocyanate  
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