本文選題：二甲基亞硝胺 + 肝纖維化�。� 參考：《延邊大學(xué)》2005年碩士論文

【摘要】：目的:探討二甲基亞硝胺誘發(fā)大鼠肝纖維化在兩個(gè)不同時(shí)間段的病理形態(tài)學(xué)特征。 方法:用1%二甲基亞硝胺腹腔注射4周誘發(fā)肝纖維化的動物模型,觀察第4周和第7(染毒停止3周后)末大鼠肝/體重比、血清門冬氨酸轉(zhuǎn)移酶、丙氨酸轉(zhuǎn)移酶活性、總蛋白和總膽固醇含量的變化;觀察肝組織的病理變化,檢測肝組織內(nèi)膠原纖維的面密度圖。免疫組化利用ED1和α-SMA抗體觀察肝組織內(nèi)枯否氏細(xì)胞和星狀細(xì)胞的表達(dá)。 結(jié)果:第4周末模型組與對照組比較血清門冬氨酸轉(zhuǎn)移酶、丙氨酸轉(zhuǎn)移酶的活性和總膽固醇的含量明顯升高,總蛋白含量明顯下降;肝/體重比明顯下降,肝組織內(nèi)膠原纖維面密度明顯升高,大部分(7/9)形成彌漫性肝硬化。免疫組化染色ED1+、α-SMA+細(xì)胞在增生的纖維間隔間大量彌漫分布,肝實(shí)質(zhì)間散在分布。第7周末模型組與對照組比較除了血清總蛋白無明顯變化外上述各項(xiàng)指標(biāo)基本與第4周模型組相似,仍保持肝硬化的特點(diǎn)。 結(jié)論:利用二甲基亞硝胺誘發(fā)的肝纖維化模型第4周末模型組大鼠肝功能明顯受損傷,大部分表現(xiàn)為彌漫性肝硬化的形態(tài)學(xué)改變;染毒停止后3周末仍保持肝硬化的形態(tài)學(xué)特點(diǎn)。二甲基亞硝胺誘發(fā)的肝纖維化動物模型,適合進(jìn)行肝纖維化的發(fā)生機(jī)制及抗肝纖維化藥物療效的研究。
[Abstract]:Objective: to investigate the pathomorphological characteristics of hepatic fibrosis induced by dimethylnitrosamine in rats at two different periods. Methods: the animal model of hepatic fibrosis induced by intraperitoneal injection of 1% dimethylnitrosamine for 4 weeks was established. The changes of liver / body weight ratio, serum aspartate transferase, alanine transferase activity, total protein and total cholesterol were observed at the end of week 4 and 7 (3 weeks after exposure), and the pathological changes of liver tissue were observed. The surface density of collagen fibers in liver tissue was measured. The expression of Kupffer cells and stellate cells in liver tissue was observed by immunohistochemical staining with ED1 and 偽 -SMA antibodies. Results: the serum aspartate transferase levels in the model group were compared with those in the control group at the end of the 4th week. The activity of alanine transferase and the content of total cholesterol increased obviously, the content of total protein decreased obviously, the ratio of liver to body weight decreased obviously, the density of collagen fibers in liver tissue increased obviously, most of them formed diffuse cirrhosis. Immunohistochemical staining showed that ED1, 偽 -SMA cells were distributed widely between proliferative fibrous septum and hepatic parenchyma. At the end of the 7th week, the above indexes in the model group were similar to those in the model group at the 4th week, except that there was no significant change in the serum total protein level between the model group and the control group. Conclusion: the hepatic fibrosis model induced by Dimethylnitrosamine at the end of the 4th week in the model group was obviously damaged, most of which were the morphological changes of diffuse cirrhosis. The morphologic features of liver cirrhosis remained at the end of 3 weeks after cessation of exposure. The animal model of hepatic fibrosis induced by Dimethylnitrosamine is suitable for studying the mechanism of hepatic fibrosis and the effect of anti-fibrosis drugs.
【學(xué)位授予單位】：延邊大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2005
【分類號】：R363

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