肝细胞糖原拮抗肝脏缺血损伤及其与细胞间黏附分子-1基因的关系  

Hepatocellular glycogen alleviates hepatic ischemia reperfusion injury and its relationship to ICAM-1 gene expression

作　　者：汤礼军[1] 田伏洲[1] 汪涛[1] 崔建峰[1] 罗皓[1] 黎冬暄[1] 石力[1] 陈涛[1] 邹树[1] 

机构地区：[1]成都军区总医院全军普通外科中心,610083

出　　处：《中华肝脏病杂志》2008年第11期858-860,共3页Chinese Journal of Hepatology

摘　　要：目的探讨肝细胞糖原在拮抗肝脏缺血再灌注损伤过程中肝窦内皮细胞细胞间黏附分子-1（ICAM-1）mRNA的表达规律及其意义。方法健康成年新西兰大耳白兔21只，随机分为3组，术前（缺血前）24h各组动物分别做以下处理：A组（n=7）：禁食24h；B组（n=7）：标准实验室饮食；C组（n=7）：标准实验室饮食加每4h静脉注射25％葡萄糖溶液20ml（共6次）。此后制备肝脏缺血再灌注损伤模型。观察各组白兔肝脏缺血再灌注过程中肝功能、肝窦腔内白细胞数量及肝窦内皮细胞表达ICAM-1 mRNA含量的变化情况。结果每克湿肝组织糖原含量为A组为（9．85±0．91）mg、B组为（38．93±5．72）mg；C组为（48．31±6．58）mg；3组白兔肝脏再灌注1h时AST：A、B、C组分别为（4J6．1±5．0）U／L、（33．8±6．3）U／L和（21．5±5．1）U／L，糖原含量越高的肝脏，肝功能损伤越轻。3组肝脏于缺血前及缺血末，肝组织内ICAM-1 mRNA含量差异无统计学意义。于再灌注60min时，糖原含量越高的肝脏，其组织内ICAM-1 mRNA含量越低，每毫克湿肝组织含量为：A组（1．398±0．365）ng、B组（0．852±0．297）ng、C组（0．366±0．183）ng，且此时肝窦腔内白细胞数量也越低。相关性分析结果显示，肝脏糖原含量与肝脏组织中ICAM-1 mRNA含量间呈显著的负相关关系（r=-0．965，P〈0．01）。结论肝细胞糖原抑制肝窦内皮细胞过量表达ICAM-1可能是其拮抗肝脏缺血再灌注损伤的重要机制。Objective To investigate if higher hepatocellular glycogen contents can alleviate hepatic ischemia reperfusion injury and its relationship to ICAM-1 gene expression in hepatic sinusoidal ceils （HSCs）. Methods Twenty-one rabbits fed with a standard diet were randomly divided into three groups （n = 7 in each）. All the animals were subjected to hepatic ischemia reperfusion injury then sacrificed. Before the injury, group A rabbits fasted for 24 hours; group C rabbits had 6 intravenous glucose solution （25%, 20 ml） injections, 4 hours between two injections. Hepatic enzymological changes, hepatic ICAM-1 mRNA expressions and leukocytic counts in the sinusoids were observed. Results The liver glycogen contents of the three groups were significantly different. Livers of group A had higher contents of glycogen （9.85±0.91 mg/g. wet tissue）; in group B they were 38.93±5.72; and in group C they were 48.31±6.58. Group C animals had the slightest liver function damage. There were no differences in the preand post-ischemiac ICAM-1 mRNA contents in the three groups. However, livers with a higher content of glycogen showed less expression of ICAM-1 mRNA （group A： 1.398±0.365 ng/mg wet tissue;group B： 0.852±0.297; group C： 0.366±0.183） and lower leukocytic counts. The relationship analysis showed a negative relationship between hepatocellular glycogen and hepatic ICAM-1 mRNA contents （r = -0.965, P 〈 0.01）. Conclusions Hepatocellular glycogen is important in protecting liver ischemiac reperfusion injury. Also hepatocellular glycogen decreases the expression of ICAM-1 mRNA of HSCs.

关 键 词：兔 糖原 缺血再灌注损伤 细胞间黏附分子 

分 类 号：R575[医药卫生—消化系统]