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低温保存-再灌注肝脏肝细胞凋亡与肝细胞糖原含量的关系及bax基因在其中的作用
引用本文:汤礼军,田伏洲,王雨,高晓美.低温保存-再灌注肝脏肝细胞凋亡与肝细胞糖原含量的关系及bax基因在其中的作用[J].中国普外基础与临床杂志,2003,10(3):226-229.
作者姓名:汤礼军  田伏洲  王雨  高晓美
作者单位:成都军区成都总医院全军普外中心肝胆病区,成都,610083
摘    要:目的 研究肝脏低温保存 再灌注期间肝细胞糖原含量与肝细胞凋亡之间的关系及bax基因在其中的作用。方法 制备糖原含量显著不同的 4组兔肝脏模型 ,根据给食方法的不同分为A组 (禁食 2 4h ,但自由饮水 )、B组 (标准实验室饮食 )、C组 (标准实验室饮食 +每 6h静脉滴注 2 5 %葡萄糖 3 0ml)及D组 (标准实验室饮食 +每 4h静脉滴注2 5 %葡萄糖 3 0ml) ,检测各组肝脏低温保存 再灌注期间肝细胞凋亡及bax基因蛋白的表达情况。结果 各组肝脏于低温保存 9h后再灌注 60min时 ,肝组织内可见明显的肝实质细胞凋亡现象 ,A、B、C、D 4组的凋亡细胞数量依次减少 ,4组间两两比较差异有统计学意义 ,各组肝细胞bax基因蛋白的表达程度与肝细胞糖原含量有密切的相关性。结论 肝脏低温保存 再灌注过程中 ,肝细胞内糖原能明显拮抗肝实质细胞凋亡的发生 ,其内在机理可能为肝细胞糖原通过抑制bax基因蛋白的表达从而达到拮抗肝实质细胞凋亡的发生。

关 键 词:低温保存  再灌注  肝脏  肝细胞凋亡  肝细胞糖原  含量  bax基因  作用
文章编号:1007-9424(2003)03-0226-04
修稿时间:2002年7月16日

Relationship Between Hepatocellular Apoptosis and Glycogen Contents During Hepatic Cold Preservation-Reperfusion and Its Mechanism
TANG Li jun,TIAN Fu zhou,WANG Yu,GAO Xiao mei.Relationship Between Hepatocellular Apoptosis and Glycogen Contents During Hepatic Cold Preservation-Reperfusion and Its Mechanism[J].Chinese Journal of Bases and Clinics In General Surgery,2003,10(3):226-229.
Authors:TANG Li jun  TIAN Fu zhou  WANG Yu  GAO Xiao mei
Institution:TANG Li jun,TIAN Fu zhou,WANG Yu,GAO Xiao mei. The PLA Centre of General Surgery,General Hospital of Chengdu Military Area,Chengdu 610083,China
Abstract:Objective To study the relationship between hepatocellular apoptosis and glycogen contents during hepatic cold preservation reperfusion and its mechanism.Methods Based on the model of four groups of rabbit livers with different hepatocellular glycogen contents, hepatocellular apoptosis and bax gene expression were observed during hepatic cold preservation reperfusion.Results Apoptotic hepatocytes were obviously found in 60 minute reperfusing livers subsequent to 9 hour cold storage, and there was significant difference in the numbers of apoptotic hepatocytes among all the groups. In the same time, there was the close relationship between the levels of bax gene expression and the glycogen contents of hepatocytes.Conclusion Intracellular abundant glycogen may significantly depress the hepatocellular apoptosis during hepatic cold preservation reperfusion by decreasing hepatocellular bax gene expression.
Keywords:Reperfusion injury    Hepatocellular apoptosis    Glycogen  
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