中华肝脏病杂志
中華肝髒病雜誌
중화간장병잡지
CHINESE JOURNAL OF HEPATOLOGY
2001年
1期
16-18
,共3页
范建高%钟岚%王国良%巫协宁%靖大道%张丕利%李明升
範建高%鐘嵐%王國良%巫協寧%靖大道%張丕利%李明升
범건고%종람%왕국량%무협저%정대도%장비리%리명승
脂肪肝%肝炎,酒精性%枯否细胞
脂肪肝%肝炎,酒精性%枯否細胞
지방간%간염,주정성%고부세포
目的 探讨枯否细胞在大鼠非酒精性脂肪性肝炎(non-alcoholic steatohepatitis, NASH)发病中的作用。方法 19只雄性SD大鼠随机分为模型组(10只)和正常组(9只),分别予高脂肪饮食和标准饮食饲养12周。HE染色观察肝组织切片病理学改变,透射电镜和溶菌酶免疫组织化学染色观察枯否细胞的数量和形态。结果模型组大鼠均出现肥胖、高脂血症伴肝细胞大泡性脂肪变、小叶内炎症细胞浸润和坏死。与正常组相比,模型组肝小叶内枯否细胞数显著增加,并呈活化状态;模型组枯否细胞变化与其肝病理学改变相一致。结论高脂饮食大鼠肝脏枯否细胞增多,并可能与其脂肪性肝炎的发病有关。
目的 探討枯否細胞在大鼠非酒精性脂肪性肝炎(non-alcoholic steatohepatitis, NASH)髮病中的作用。方法 19隻雄性SD大鼠隨機分為模型組(10隻)和正常組(9隻),分彆予高脂肪飲食和標準飲食飼養12週。HE染色觀察肝組織切片病理學改變,透射電鏡和溶菌酶免疫組織化學染色觀察枯否細胞的數量和形態。結果模型組大鼠均齣現肥胖、高脂血癥伴肝細胞大泡性脂肪變、小葉內炎癥細胞浸潤和壞死。與正常組相比,模型組肝小葉內枯否細胞數顯著增加,併呈活化狀態;模型組枯否細胞變化與其肝病理學改變相一緻。結論高脂飲食大鼠肝髒枯否細胞增多,併可能與其脂肪性肝炎的髮病有關。
목적 탐토고부세포재대서비주정성지방성간염(non-alcoholic steatohepatitis, NASH)발병중적작용。방법 19지웅성SD대서수궤분위모형조(10지)화정상조(9지),분별여고지방음식화표준음식사양12주。HE염색관찰간조직절편병이학개변,투사전경화용균매면역조직화학염색관찰고부세포적수량화형태。결과모형조대서균출현비반、고지혈증반간세포대포성지방변、소협내염증세포침윤화배사。여정상조상비,모형조간소협내고부세포수현저증가,병정활화상태;모형조고부세포변화여기간병이학개변상일치。결론고지음식대서간장고부세포증다,병가능여기지방성간염적발병유관。
Objective To explore the role of Kupffer cells in non-alcoholic steatohepatitis (NASH) by means of rat model. Methods Nineteen male SD rats were randomized into model group (n=10) and normal group (n=9), with a high-fat diet and standard diet for 12 weeks, respectively. Routine histologic features of hepatic section were observed by HE staining. The number and shape of Kupffer cells in the liver were detected by immunohistochemistry and penetrated electron microscope, respectively. Results All rats of model group developed NASH, which was characterized by obesity and hyperlipidemia. Histopathological examination showed hepatocellular macrovesicular steatosis, lobular inflammatory cell infiltration and necrosis. Compared with normal group, the count of Kupffer cells in the liver was largely increased, and the Kupffer cells in the model group were activated to some extent. Furthermore, these changes of Kupffer cells were in accordance with the degree of steatosis, inflammation and necrosis in the liver of the model group. Conclusion The number and activity of Kupffer cells are increased significantly in NASH induced by high-fat diet, and Kupffer cells might be involved in the pathogenesis of steatohepatitis.