库普弗细胞异常在大鼠非酒精性脂肪肝病发生发展中的作用  

The role of Kupffer cells disorder on the occurrence and development of Nonalcoholic Fatty Liver Disease in rats

作　　者：贺丹[1,2] 刘慧霞[1] 李岚[1] 谭雅琴[1] 

机构地区：[1]中南大学湘雅医院老年病科,湖南长沙410008 [2]湖南省湘潭市中心医院内分泌科

出　　处：《中国医师杂志》2009年第12期1585-1588,共4页Journal of Chinese Physician

基　　金：国家自然科学基金资助项目（30670945）;国家人事部留学人员科技活动项目择优资助经费项目（2006-164）;湖南省自然科学基金资助项目（07JJ5108）

摘　　要：目的探讨库普弗细胞（KCs）异常在高脂饲养大鼠非酒精性脂肪肝病（NAFLD）发病中的作用。方法24只雄性SD大鼠随机分为模型组和正常组各12只，分别予高脂饲料和普通饲料饲养12周。然后测定体重、肝重、空腹血清丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、甘油三酯（TG）、总胆固醇（TC）水平；HE染色观察肝组织切片病理学改变，并观察KCs形态变化及分泌肿瘤坏死因子-α（TNF-α）、一氧化氮（NO）的水平。结果模型组大鼠体重、肝指数、血清ALT、AST、TG、TC水平、肝脏KCs产生的TNF-α及NO水平均高于正常组（P〈0．05）；与正常组相比，模型组肝小叶内KCs发生形态及功能改变，该变化与肝组织病理学改变呈正相关（r=0．702，0．810，0．587，0．765，P均〈0．05）。结论高脂饮食大鼠肝脏库普弗细胞呈现形态及功能异常，该异常可能与NAFLD脂肪变性及炎症坏死的发生有关。Objective To explore the role of Kupffer cells （KCs）disorder on the occurrence and development of Nonalcoholic Fatty Liver Disease （NAFLD） by means of rat model fed with high-fat diet. Methods Twenty-four male SD rats were random divided into model group （ n = 12） and normal group（ n = 12）, with a high-fat diet and standard diet for 12 weeks. The levels of body weight, liver weight, alanine aminotransferase （ ALT）, aspartate aminotransferase （ AST）, triglyceride （ TG）, and total cholesterol （ TC ） were measured. Routine histological features of hepatic section were observed by H. E staining. The shape changes of KCs in the liver were detected, and the levels of tumor necrosis factor-α（TNF-α） and nitric oxide （NO） secreted by KCs were measured. Results The weight, liver index, the levels of ALT, AST, TG, TC, and the levels of TNF-α and NO secreted by KCs in model group were higher than that in the normal group （ P 〈 0. 05）. Histopathological examination showed hepatocellular macrovesicular steatosis, lobular inflammatory cell infiltration and necrosis. Compared with normal group, the shape and function of KCs in the liver changed largely. Furthermore, these changes of KCs were in accordance with the degree of steatosis, inflammation and necrosis in the liver of the model group. Conclusions The shape and function of KCs changed significantly in NAFLD induced by high-fat diet, and KCs disorder might be involved in the pathogenesis of NAFLD.

关 键 词：枯否细肜病理学 脂肪肝/病理学 

分 类 号：R575[医药卫生—消化系统]