本文選題：Periostin + 蛋氨酸膽堿缺乏的飼料��； 參考：《廈門(mén)大學(xué)》2014年碩士論文

【摘要】：非酒精性脂肪肝炎是指除酒精、病毒和遺傳性等因素之外所導(dǎo)致的脂肪性肝炎,即肝臟中超過(guò)5%～10%的肝細(xì)胞中發(fā)生脂質(zhì)累積的現(xiàn)象,并且還伴隨有炎癥和纖維化現(xiàn)象。非酒精性脂肪肝炎可以進(jìn)一步惡化形成肝硬化,甚至肝癌。雖然對(duì)非酒精性脂肪肝炎的病理機(jī)制已有大量的研究,但是其發(fā)生機(jī)制仍然沒(méi)有得到確切闡明。Periostin作為一種細(xì)胞外基質(zhì)蛋白,不僅在發(fā)育、組織修復(fù)、腫瘤發(fā)生發(fā)展過(guò)程中起著重要作用,而且與一些炎癥性疾病如哮喘、肺炎等也具有密切關(guān)系,但是有關(guān)Periostin在肝炎當(dāng)中的作用目前還未有報(bào)道。本研究主要探討了Periostin在非酒精性脂肪肝炎中的作用。我們發(fā)現(xiàn)在MCD飼料誘導(dǎo)C57BL/6小鼠發(fā)生非酒精脂肪肝炎后,小鼠肝臟中Periostin的表達(dá)量升高,但Periostin基因敲除小鼠與同窩對(duì)照組相比,NASH現(xiàn)象明顯減輕。0.2mM棕櫚酸鹽處理人正常肝細(xì)胞系QSG7701發(fā)生脂質(zhì)堆積現(xiàn)象；其條件培養(yǎng)基可誘導(dǎo)人肝臟星形細(xì)胞系LX-2表達(dá)Periostin。另外,體外過(guò)表達(dá)Periostin的QSG7701細(xì)胞在0.2mM棕櫚酸鹽處理后,其PPARy表達(dá)水平相對(duì)于對(duì)照組明顯上升。因此,這些結(jié)果表明Periostin參與了MCD飼料模型誘導(dǎo)的非灑精性脂肪肝炎的發(fā)生發(fā)展過(guò)程。
[Abstract]:Non-alcoholic fatty liver disease is a kind of fatty hepatitis caused by alcohol, virus and heredity, that is, lipid accumulation occurs in more than 5% of liver cells and accompanied by inflammation and fibrosis. Non-alcoholic fatty liver disease can further worsen the formation of liver cirrhosis, and even liver cancer. Although a great deal of research has been done on the pathological mechanism of non-alcoholic fatty liver disease, the pathogenesis of nonalcoholic fatty liver disease has not been clarified exactly. Periostin, as an extracellular matrix protein, is not only in development, but also in tissue repair. Tumor plays an important role in tumorigenesis and development, and is closely related to some inflammatory diseases such as asthma and pneumonia. However, the role of Periostin in hepatitis has not been reported. The purpose of this study was to investigate the role of Periostin in non-alcoholic fatty liver disease. We found that the expression of Periostin in the liver of C57BL / 6 mice increased after MCD diet induced non-alcoholic fatty liver inflammation. Compared with the control group, Periostin gene knockout mice significantly reduced lipid accumulation in human normal liver cell line QSG7701 treated with 0.2mm palmitate, and its conditioned medium could induce the expression of Periostinin in human hepatic stellate cell line LX-2. In addition, the expression level of PPARy in QSG7701 cells treated with 0.2 mm palmitate was significantly higher than that in control group. Therefore, these results suggested that Periostin was involved in the development of non-spermatogenic fatty hepatitis induced by MCD feed model.
【學(xué)位授予單位】：廈門(mén)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類(lèi)號(hào)】：R575.5

【參考文獻(xiàn)】

相關(guān)期刊論文 前2條

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2 Duangporn Thong-Ngam;Suchittra Samuhasaneeto;Onanong Kulaputana;Naruemon Klaikeaw;;N-acetylcysteine attenuates oxidative stress and liver pathology in rats with non-alcoholic steatohepatitis[J];World Journal of Gastroenterology;2007年38期

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本文編號(hào)：2075930