中国医药科学
中國醫藥科學
중국의약과학
CHINA MEDICINE AND PHARMACY
2013年
16期
25-26,76
,共3页
非酒精性脂肪肝%UCP2%动态表达
非酒精性脂肪肝%UCP2%動態錶達
비주정성지방간%UCP2%동태표체
Non-alcoholic fatty liver disease%UCP2%Dynamic expression
目的探讨大鼠非酒精性脂肪肝中UCP2的动态表达,进一步明确其在非酒精性脂肪肝中的发病机制。方法选取大鼠60只进行实验,按照随机分组原则划分为观察组和对照组,观察组采用高脂饮食进行脂肪肝诱导,采用免疫组织学技术和Western blot技术对大鼠肝组织中的UCP2进行检测,对大鼠的血清甘油三脂(TG)、丙氨酸氨基转移酶(ALT)和游离脂肪酸(FFA)含量进行检测。结果大鼠在形成非酒精性脂肪肝过程中,体内UCP2阳性细胞的含量以及TG、ALT、FAA的表达和含量都会显著增加,在高脂饮食诱导8~12周期间最为明显。结论大鼠非酒精性脂肪肝的形成与发展程度与体内UCP2表达强度呈正比例关系,UCP2的酶活性增高会导致促进脂质过氧化反应,促进脂肪肝的形成。
目的探討大鼠非酒精性脂肪肝中UCP2的動態錶達,進一步明確其在非酒精性脂肪肝中的髮病機製。方法選取大鼠60隻進行實驗,按照隨機分組原則劃分為觀察組和對照組,觀察組採用高脂飲食進行脂肪肝誘導,採用免疫組織學技術和Western blot技術對大鼠肝組織中的UCP2進行檢測,對大鼠的血清甘油三脂(TG)、丙氨痠氨基轉移酶(ALT)和遊離脂肪痠(FFA)含量進行檢測。結果大鼠在形成非酒精性脂肪肝過程中,體內UCP2暘性細胞的含量以及TG、ALT、FAA的錶達和含量都會顯著增加,在高脂飲食誘導8~12週期間最為明顯。結論大鼠非酒精性脂肪肝的形成與髮展程度與體內UCP2錶達彊度呈正比例關繫,UCP2的酶活性增高會導緻促進脂質過氧化反應,促進脂肪肝的形成。
목적탐토대서비주정성지방간중UCP2적동태표체,진일보명학기재비주정성지방간중적발병궤제。방법선취대서60지진행실험,안조수궤분조원칙화분위관찰조화대조조,관찰조채용고지음식진행지방간유도,채용면역조직학기술화Western blot기술대대서간조직중적UCP2진행검측,대대서적혈청감유삼지(TG)、병안산안기전이매(ALT)화유리지방산(FFA)함량진행검측。결과대서재형성비주정성지방간과정중,체내UCP2양성세포적함량이급TG、ALT、FAA적표체화함량도회현저증가,재고지음식유도8~12주기간최위명현。결론대서비주정성지방간적형성여발전정도여체내UCP2표체강도정정비례관계,UCP2적매활성증고회도치촉진지질과양화반응,촉진지방간적형성。
Objective To discuss the dynamic expression of UCP2 in rat's non-alcoholic fatty liver disease and specify its pathogenesis in non-alcoholic fatty liver disease. Methods 60 rats were chosen for the experiment, which were randomly divided into the observation group and control group. In the observation group, rats received the high-fat diet for the induction of fatty liver and the immune histological technique and Western blot technique were adopted to measure UCP2 in rat's liver and contents of triglyceride (TG), alanine transaminase (ALT) and free fatty acid (FFA). Results During the formation of non-alcoholic fatty liver disease, the content of UCP2 positive cells and expression and contents of TG, ALT and FFA in rats were significantly increased, which were most obvious during 8th-12th week of induction of high-fat diet. Conclusion The formation and development of rat's non-alcoholic fatty liver disease is proportional to the expression of UCP2. The increased enzymatic activity of UCP2 will accelerate the lipid peroxidation and promote the formation of fatty liver.