CAJ | 학술논문

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(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擎改变呈正相关(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.
목적 탐토고보불세포(KCs)이상재고지사양대서비주정성지방간병(NAFLD)발병중적작용.방법 24지웅성SD대서수궤분위모형조화정상조각12지,분별여고지사료화보통사료사양12주.연후측정체중、간중、공복혈청병안산안기전이매(ALT)、천문동안산안기전이(AST)、감유삼지(TG)、총담고순(TC)수평;HE염색관찰간조직절편병이학개변,병관찰KCs형태변화급분비종류배사인자-α(TNF-α)、일양화담(NO)적수평.결과 모형조대서체중、간지수、혈청ALT、AST、TG、TC수평、간장Kcs산생적TNF-α급NO수평균고우정상조(P<0.05);여정상조상비,모형조간소협내KCs발생형태급공능개변,해변화여간조직병리경개변정정상관(r=0.702,0.810,0.587,0.765,P균<0.05).결론 고지음식대서간장고보불세포정현형태급공능이상,해이상가능여NAFLD지방변성급염증배사적발생유관.
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.