發(fā)布時(shí)間：2018-06-21 03:33

  本文選題：肝源磷脂酰膽堿 + CC14肝損傷��； 參考：《遼寧師范大學(xué)》2006年碩士論文

【摘要】：磷脂酰膽堿(Phosphatidylcholine，PC)也稱卵磷脂。它是細(xì)胞膜的重要組成成分，起保護(hù)層的作用，能重新修復(fù)由于自由基攻擊生物大分子而產(chǎn)生的膜損傷；它具有膽堿成分，膽堿對(duì)脂肪具有親和力，可使脂肪以磷脂形式由肝臟通過(guò)血液輸送出去，從而防止脂肪肝的形成；它是提供神經(jīng)物質(zhì)乙酰膽堿的前體物質(zhì)，具有健腦功能；還用于脂質(zhì)體的研究，以及作為抗癌藥物的研究，在食品、醫(yī)藥、化妝品等領(lǐng)域有廣闊的應(yīng)用前景。 肝臟是人體代謝的中心站，含有極其豐富的PC。在哺乳動(dòng)物肝臟中，除了CDP-膽堿通路(又稱Kennedy通路)外，還存在一條特有的PC合成通路，即磷脂酰乙醇胺N-甲基轉(zhuǎn)移酶(phosphatidylethanolamine N-methyltransferase，PEMT)催化磷脂酰乙醇胺(phosphorylethanolamine，PE)甲基化生成PC的通路。研究發(fā)現(xiàn)，肝病時(shí)合成PC的PEMT活性降低。我們實(shí)驗(yàn)室利用基因轉(zhuǎn)染技術(shù)過(guò)表達(dá)PEMT2后，發(fā)現(xiàn)大鼠肝癌細(xì)胞的生長(zhǎng)被顯著抑制，并誘發(fā)其細(xì)胞凋亡。提示，肝臟中的PC可能具有獨(dú)特的作用。有研究表明，肝細(xì)胞損傷時(shí)，細(xì)胞膜的PC代謝和含量會(huì)發(fā)生明顯的變化。那么，補(bǔ)充外源肝性的PC是否有利于受損傷的肝細(xì)胞恢復(fù)或減輕肝損傷的程度? CCl_4是目前建立肝細(xì)胞實(shí)驗(yàn)性損傷模型的常用藥物，能成功的復(fù)制肝損傷模型。CCl_4可通過(guò)P-450酶系統(tǒng)脫鹵素后形成CCl_3自由基，后者能從不飽和脂肪酸分子中奪取氫離子，引起脂質(zhì)過(guò)氧化。本研究以CCl_4誘導(dǎo)正常人肝細(xì)胞HL7702損傷，復(fù)制肝細(xì)胞損傷模型，，觀察了補(bǔ)充肝源PC對(duì)肝
[Abstract]:Phosphatidylcholine Phosphatidylcholine (PCP) is also known as lecithin. It is an important component of the cell membrane and acts as a protective layer that restores membrane damage caused by free radicals attacking biomolecules; it has a choline component, and choline has affinity for fat. Fat is transported through the blood by the liver in the form of phospholipid, thus preventing the formation of fatty liver; it is a precursor material to provide the nerve substance acetylcholine and has the function of strengthening the brain; it is also used in the study of liposome. As well as the research of anticancer drugs, it has broad application prospect in food, medicine, cosmetics and so on. The liver is the center of human metabolism, containing extremely rich PCS. In mammalian livers, in addition to the CDP- choline pathway (also known as Kennedy pathway), there is a unique PC synthesis pathway. Phosphatidylethanolamine N-methyltransferase (PEMT) catalyzes the methylation of phosphatidylethanolamine to PC. It was found that the PEMT activity of PC was decreased during liver disease. After overexpression of PEMT2 by gene transfection technique in our laboratory, we found that the growth of rat hepatoma cells was significantly inhibited and apoptosis induced. These results suggest that PC may play a unique role in the liver. Some studies have shown that the metabolism and content of PC in the cell membrane change obviously when the liver cell is damaged. So, is supplementation of exogenous hepatic PC beneficial to the recovery of the injured hepatocytes or the reduction of the degree of liver injury? CClst4 is a common drug used to establish experimental liver injury model. CClS4 can successfully replicate the liver injury model. CClS4 can dehalogenate through P-450 enzyme system to form CCl3 free radical, which can capture hydrogen ion from fatty acid molecule. Cause lipid peroxidation. In this study, normal human hepatocytes HL7702 were induced by CClS4, and the model of hepatocyte injury was established. The effects of liver PC supplementation on liver were observed.
【學(xué)位授予單位】：遼寧師范大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：R363

【引證文獻(xiàn)】

相關(guān)碩士學(xué)位論文 前1條

1 梁偉;牡蠣湯對(duì)CCL_4誘發(fā)大鼠慢性肝損傷保護(hù)作用的實(shí)驗(yàn)研究[D];黑龍江中醫(yī)藥大學(xué);2008年

本文編號(hào)：2047015