端粒酶RNA基因Terc在非酒精性脂肪性肝病中的作用機(jī)制研究
發(fā)布時間：2019-06-19 23:31
【摘要】：目的：非酒精性脂肪性肝病(NAFLD)是臨床常見的慢性肝病,其發(fā)病機(jī)制尚未完全明確。研究發(fā)現(xiàn),衰老與NAFLD的發(fā)生與發(fā)展密切相關(guān),而端粒酶RNA基因Terc在衰老發(fā)生中起到重要的作用。然而,Terc是否參與NAFLD的發(fā)生發(fā)展及其確切分子機(jī)制尚未報道。本研究旨在通過體內(nèi)實驗的方法,探討端粒酶RNA基因Terc在NAFLD的發(fā)生發(fā)展中可能的作用機(jī)制。方法：本研究采用蛋氨酸-膽堿缺乏(MCD)飲食飼養(yǎng)第二代端粒酶基因敲除小鼠(G2Terc-/-)與正常小鼠,在此基礎(chǔ)上,采用蘇木素-伊紅(HE)染色,肝組織甘油三酯含量測定及熒光定量PCR等分子生物學(xué)手段,探討端粒酶RNA基因Terc在NAFLD發(fā)生發(fā)展中的作用及分子機(jī)制。結(jié)果：(1)用MCD飲食成功構(gòu)建NAFLD動物模型(2)第二代端粒酶基因敲除小鼠(G2 Terc-/-)顯著增加MCD飲食誘導(dǎo)的肝組織脂肪沉積；而且G2 Terc-/-小鼠組肝臟甘油三酯含量高于野生型(WT)小鼠組(172.5μg/mg比150μg/mg) (P=0.018)(3)第二代端粒酶基因敲除小鼠(G2Terc-/-)組的脂質(zhì)合成基因脂肪酸合成酶(FAS)表達(dá)高于野生型(WT)小鼠組(P=0.026),導(dǎo)致脂質(zhì)合成增加(4)第二代端粒酶基因敲除小鼠(G2 Terc-/-)組的脂肪酸p氧化基因過氧化物酶體增殖物激活受體α表達(dá)低于野生型小鼠(WT)組(P=0.050),導(dǎo)致脂肪酸p氧化受損。結(jié)論：(1) Terc參與NAFLD的發(fā)生發(fā)展；(2) Terc基因缺失可能通過上調(diào)FAS基因及下調(diào)PPARa基因表達(dá)參與NAFLD發(fā)生和發(fā)展。
[Abstract]:Objective: non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease in clinic, and its pathogenesis is not completely clear. It was found that aging was closely related to the occurrence and development of NAFLD, and telomerase RNA gene Terc played an important role in senescence. However, it has not been reported whether Terc is involved in the occurrence and development of NAFLD and its exact molecular mechanism. The purpose of this study was to explore the possible mechanism of telomerase RNA gene Terc in the occurrence and development of NAFLD by means of in vivo experiments. Methods: the second generation telomerase gene knockout mice and normal mice were fed with methionine choline deficient (MCD) diet. On this basis, the role and molecular mechanism of telomerase RNA gene Terc in the occurrence and development of NAFLD were investigated by hematoxylin-eosin (HE) staining, determination of TG content in liver tissue and fluorescence quantitative PCR. Results: (1) the animal model of NAFLD was successfully constructed by MCD diet. (2) the second generation telomerase gene knockout mice (G2 Terc-/-) significantly increased the fat deposition of liver tissue induced by MCD diet. The content of TG in liver of G2Tercg mice was higher than that of wild type (WT) mice (172.5 渭 g / mg vs 150 渭 g / mg) (P 鈮，
本文編號：2502721
[Abstract]:Objective: non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease in clinic, and its pathogenesis is not completely clear. It was found that aging was closely related to the occurrence and development of NAFLD, and telomerase RNA gene Terc played an important role in senescence. However, it has not been reported whether Terc is involved in the occurrence and development of NAFLD and its exact molecular mechanism. The purpose of this study was to explore the possible mechanism of telomerase RNA gene Terc in the occurrence and development of NAFLD by means of in vivo experiments. Methods: the second generation telomerase gene knockout mice and normal mice were fed with methionine choline deficient (MCD) diet. On this basis, the role and molecular mechanism of telomerase RNA gene Terc in the occurrence and development of NAFLD were investigated by hematoxylin-eosin (HE) staining, determination of TG content in liver tissue and fluorescence quantitative PCR. Results: (1) the animal model of NAFLD was successfully constructed by MCD diet. (2) the second generation telomerase gene knockout mice (G2 Terc-/-) significantly increased the fat deposition of liver tissue induced by MCD diet. The content of TG in liver of G2Tercg mice was higher than that of wild type (WT) mice (172.5 渭 g / mg vs 150 渭 g / mg) (P 鈮，
本文編號：2502721
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