本文選題：miR-206 + 肝臟X受體α�。� 參考：《山西醫(yī)科大學(xué)》2015年碩士論文

【摘要】：目的:本實驗通過構(gòu)建apo E-KO小鼠動脈粥樣硬化模型,探討mi R-206對apo E-KO動脈粥樣硬化小鼠肝臟膽固醇逆轉(zhuǎn)運相關(guān)蛋白肝臟X受體α表達和膽固醇流出率的影響,進一步研究mi R-206參與膽固醇逆轉(zhuǎn)運的機制。方法:高脂飲食喂養(yǎng)apo E-KO小鼠30只,建立動脈粥樣硬化模型。將小鼠隨機平均分為3組,A組:PBS對照組;B組:mi R-206 mimic組;C組:mi R-206 inhibitor組。分別于腹腔皮下注射PBS溶液、mi R-206 mimic溶液、mi R-206 inhibitor溶液。4周后,眶靜脈取血檢測血脂水平,取主動脈根部HE染色及油紅O染色觀察動脈粥樣硬化程度,熒光定量RT-PCR和Western-blot法檢測各組小鼠肝臟m RNA相對表達量和蛋白含量,液態(tài)閃爍計數(shù)法檢測各組小鼠腹腔巨噬細胞膽固醇的流出率。結(jié)果:mi R-206 mimic組較對照組HDL-C水平升高;與對照組、mi R-206 mimic組相比,mi R-206 inhibitor組TC、LDL均顯著升高,HDL明顯下降。各組TG無明顯不同。主動脈根部行HE染色、油紅O染色可見對照組粥樣硬化程度較輕,mi R-206inhibitor組動脈粥樣硬化程度最為嚴重,mi R-206 mimic組動脈粥樣硬化病變極其微小。與對照組相比,mi R-206 mimic組肝LXRαm RNA和蛋白表達增多,mi R-206inhibitor組表達減少。膽固醇流出率的結(jié)果顯示,mi R-206 mimic組百分率的較對照組的明顯升高,mi R-206 inhibitor組較對照組明顯下降。結(jié)論:mi R-206與LXRα之間可能有中間物質(zhì)的參與,構(gòu)成了反饋環(huán),作為LXR活性自身調(diào)控的一部分,共同調(diào)節(jié)膽固醇逆轉(zhuǎn)運的過程。
[Abstract]:Aim: to investigate the effects of miR-206 on the expression of cholesterol reverse transporter associated protein X receptor 偽 and cholesterol efflux rate in the liver of apo E-KO mice by establishing an atherosclerosis model of apo E-KO mice. To further study the mechanism of mi R-206 involved in cholesterol reverse transport. Methods: 30 apo E-KO mice were fed with high fat diet to establish atherosclerosis model. The mice were randomly divided into three groups: group A, control group, group B, group C, group 鈪，

本文編號：2096418