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| Establishment of early experimental model for liver injury of alcoholism in rats |
| CHEN Huan1 LIU Yan-ling1 LIU Xue-rui1 CAI Si-yu1 WANG Jia-min1 LIU Lan2▲ |
1.Basic Medicine Department,Southwest Medical University,Sichuan Province,Luzhou 646000,China;
2.Department of Cell Biology and Genetics,Southwest Medical University,Sichuan Province,Luzhou 646000,China |
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Abstract ObjectiveTo explore the method of establishing a model of early alcoholic liver disease （ALD）in rats in order to provide an ideal animal model for studying the molecular mechanism of early alcoholic liver injury.MethodsTwenty-four male SD rats were randomly divided into experimental group (16 rats)and control group (8 rats).In the control group,SD rats were fed with tap water.In the experimental group,SD rats were fed with alcohol of which the concentration of 7%-56%increased gradually for 12 weeks.During the experiment,the quantity of the fodder and the value of drinking were recorded everyday.Then the weight was weighed every week.24 and 12 hours before rats in experimental group were killed,they were treated with acute lavages with 56%alcohol.The activities of alanine aminotransferase （ALT）,spartate aminotransferase （AST）,riglyceride （TG） and total cholesterol （TC） in serum were determined by the fully automatic biochemical analyser.Moreover,the histological and morphological changes of liver tissues were observed.ResultsThe growth rate of body mass was （160.09±3.12）%in the control group at the end of 12thweek,while it was（61.67±1.98）%in the experimental group （P＜0.05）.The ratio of liver body weight of the experimental group （3.74±0.54） was obviously increased compared with the control group （2.85±1.26）（P＜0.05）.Compared with the control group,the levels of AST,ALT,TG and TC of the model group were clearly increased （P＜0.05）.Meanwhile,the typical fatty liver pathologic changes,local inflammation and necrosis were observed in experimental group.ConclusionThe results show that the ALD model with low mortality is stable and easy to copy,which is highly similar to the early ALD in human,and can be used in the study of ALD.
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| [1] |
Gao B，Bataller R.Alcoholic liver disease：pathogenesis and new therapeutic targets[J].Gastroenterology，2011，141（5）：1572-1585.
|
| [2] |
Bruha R，Dvorak K，Petrtyl J.Alcoholic liver disease[J].World J Hepatol，2012，4（3）：81-90.
|
| [3] |
周恒，李俊，王华.酒精性肝病动物模型研究进展[J].中国药理学通报，2016，32（4）：468-472.
|
| [4] |
中华医学会肝病学分会脂肪肝和酒精性肝病学组.酒精性肝病诊疗指南（2010年修订版）[J].中华肝脏病杂志，2010，18（3）：167-170.
|
| [5] |
Wang FS，Fan JG，Zhang Z，et al.The global burden of liver disease：the major impact of China[J].Hepatology，2014，60（6）：2099-2108.
|
| [6] |
王玲，孙妩弋，魏伟，等.酒精性肝病动物模型的研究进展[J].安徽医药，2010，14（7）：745-748.
|
| [7] |
郭俊英，刘光亮，李月芬，等.酒精诱发大鼠肝损伤的分子机制与蛋白质组学研究[J].现代医药卫生，2012，28（1）：14-17.
|
| [8] |
李鑫，王晨，聂娇，等.酒精性肝炎小鼠肝肠组织变化与内毒素血症的关系探讨[J].实用肝脏病杂志，2013，16（3）：254-256.
|
| [9] |
孙希良，吕冠华，杨杰，等.益肝颗粒对酒精性肝损伤大鼠保护作用的实验研究[J].中国中西医结合消化杂志，2014，22（1）：10-12.
|
| [10] |
汤小刚，洪汝涛.水提乌药与醇提乌药对急性酒精性肝损伤模型大鼠的保护作用[J].中国临床药理学杂志，2016，32（8）：703-706.
|
| [11] |
Maricic I，Sheng H，Marrero I，et al.Inhibition of type Ⅰnatural killer T cells by retinoids or following sulfatidemediated activation of typeⅡnatural killer T cells attenuates alcoholic liver disease in mice[J].Hepatology，2015，61（4）：1357-1369.
|
| [12] |
Cui K，Yan G，Xu C，et al.Invariant NKT cells promote alcohol-induced steatohepatitis through interleukin-1 beta in mice[J].J Hepatol，2015，62（6）：1311-1318.
|
| [13] |
万远太，陈瑶.Cystatin C在大鼠酒精性肝病中的表达及意义[J].胃肠病学和肝病学杂志，2011，20（7）：624-627.
|
| [14] |
程海涛.肝脏酶谱对肝病类型及预后的临床诊断价值研究[J].现代诊断与治疗，2015，26（2）：419-420.
|
| [15] |
袁世伟，郑卫东.肝脏酶谱检测在诊断肝病中的应用及其临床意义[J].临床和实验医学杂志，2012，11（23）：1884-1885.
|
| [16] |
仝君，童师雯，王丹，等.HBV感染者血清AST/ALT比值及HBV血清标志物联合检测的辅助诊断价值研究[J].标记免疫分析与临床，2011，18（1）：8-11.
|
| [17] |
曹智丽，周俊英，王娟，等.酒精性肝病大鼠肝组织PPARα 表达及意义[J].山东医药，2016，56（24）：31-33.
|
| [18] |
郭丽英，李亚敏，李青春.酒精性脂肪肝大鼠模型肝组织中HIFs/PPAR信号通路激活程度与脂质代谢的关系[J].海南医学院学报，2015，21（11）：1459-1462.
|
| [19] |
邬升，郑世华，仝巧云.酒精性肝病发病机制的研究进展[J].实用医学杂志，2013，29（12）：2049-2050.
|
| [20] |
杨万枝.酒精性肝病发病机制研究进展[J].安徽医科大学学报，2012，47（1）：97-99.
|
|
|
|
