本文選題：乙醛脫氫酶2 + 動(dòng)脈粥樣硬化��； 參考：《山東大學(xué)》2017年碩士論文

【摘要】：研究背景動(dòng)脈粥樣硬化是心、腦血管和外周血管疾病中首要的發(fā)病病因。動(dòng)脈粥樣硬化由高血壓、高血脂、吸煙、糖尿病等多種危險(xiǎn)因素作用引起,其病理生理的發(fā)生發(fā)展過程復(fù)雜,其中脂質(zhì)代謝障礙與紊亂公認(rèn)為動(dòng)脈粥樣硬化病理學(xué)基礎(chǔ)。在動(dòng)脈粥樣硬化初始發(fā)病過程中,脂質(zhì)沉積于血管壁,巨噬細(xì)胞募集并進(jìn)入血管內(nèi)皮下基質(zhì)吞噬脂質(zhì),從而分化為泡沫細(xì)胞,形成早期動(dòng)脈粥樣硬化斑塊中的脂質(zhì)條紋。在動(dòng)脈粥樣硬化晚期,泡沫細(xì)胞發(fā)生壞死或凋亡,造成脂質(zhì)外泄而形成壞死核心,增加斑塊的不穩(wěn)定性。所以,泡沫細(xì)胞的發(fā)生與發(fā)展貫穿動(dòng)脈粥樣硬化的病理生理過程。乙醛脫氫酶2(Aldehyde dehydrogenase 2,ALDH2)是定位在線粒體上的一種醛類物質(zhì)代謝酶,野生型的ALDH2酶活性高而突變型的ALDH2酶活性降低或失活。近年來(lái),流行病學(xué)研究顯示ALDH2參與至急性動(dòng)脈綜合征和冠狀動(dòng)脈粥樣硬化性心臟病中。來(lái)自日本、中國(guó)和韓國(guó)的幾項(xiàng)研究證明ALDH2突變型與心肌梗死、急性冠脈綜合癥等心血管疾病緊密相關(guān)。在2012年,一項(xiàng)全基因組關(guān)聯(lián)分析對(duì)ALDH2基因多態(tài)性和冠心病進(jìn)行研究,證實(shí)突變型ALDH2的人群高發(fā)冠脈綜合癥和冠狀動(dòng)脈粥樣硬化性疾病。既往研究表明ALDH2在內(nèi)皮細(xì)胞和心肌細(xì)胞保護(hù)等方面發(fā)揮重要的作用,但是ALDH2在泡沫細(xì)胞中的作用尚未有相關(guān)研究報(bào)道。在本課題組的前期研究中,我們發(fā)現(xiàn)利用慢病毒敲除ALDH2的小鼠表現(xiàn)出更多的頸動(dòng)脈動(dòng)脈粥樣硬化斑塊,其中脂質(zhì)沉積明顯增多。在本實(shí)驗(yàn)中,我們同樣證實(shí)了 ALDH2敲除小鼠在主動(dòng)脈根部也表現(xiàn)出更多的脂質(zhì)沉積。由于泡沫細(xì)胞是動(dòng)脈粥樣硬化斑塊中脂質(zhì)沉積必不可缺的一部分,同時(shí),近幾年來(lái)ALDH2的研究都表明其在心血管系統(tǒng)上發(fā)揮著重要的作用,所以我們假設(shè)ALDH2在泡沫細(xì)胞中發(fā)揮了重要的作用并依此在動(dòng)物體內(nèi)和體外的相關(guān)驗(yàn)證實(shí)驗(yàn)。研究目的1.研究ALDH2對(duì)動(dòng)脈粥樣硬化脂質(zhì)沉積的影響。2.探討ALDH2在泡沫細(xì)胞中調(diào)控脂質(zhì)沉積的機(jī)制,為動(dòng)脈粥樣硬化的病理生理過程提供進(jìn)一步的理論支持。研究方法1.乙醛脫氫酶2缺乏小鼠的脂質(zhì)沉積的變化1.1 ALDH2基因缺乏增加動(dòng)脈粥樣硬化斑塊中的脂質(zhì)ApoE-/-小鼠高脂喂養(yǎng)構(gòu)建動(dòng)脈粥樣硬化模型,利用慢病毒干擾小鼠ALDH2表達(dá)。把老鼠隨機(jī)分組分為ALDH2缺乏的實(shí)驗(yàn)組與ALDH2正常的對(duì)照組。取小鼠主動(dòng)脈根部動(dòng)脈粥樣硬化斑塊制成冰凍切片,并用油紅O染色檢測(cè)脂質(zhì)含量。1.2ALDH2影響泡沫細(xì)胞的形成1.2.1 ALDH2敲基因小鼠腹腔巨噬細(xì)胞的提取與鑒定利用ALDH2敲基因小鼠與野生小鼠作為巨噬細(xì)胞供體,在thioglycollate刺激下提取小鼠腹腔原代巨噬細(xì)胞。用細(xì)胞免疫熒光方法鑒定腹腔巨噬細(xì)胞與ALDH2的表達(dá)情況。1.2.2 ALDH2缺乏對(duì)泡沫細(xì)胞形成的影響小鼠原代巨噬細(xì)胞分為ALDH2缺乏組(ALDH2-/-)與對(duì)照組(ALDH2+/+)。分別加入氧化低密度脂蛋白刺激后,利用油紅O進(jìn)行脂質(zhì)染色,鏡下觀察并計(jì)數(shù)泡沫細(xì)胞形成。1.2.3 ALDH2缺乏對(duì)泡沫細(xì)胞內(nèi)脂質(zhì)沉積的影響小鼠原代巨噬細(xì)胞加入氧化低密度脂蛋白作用后,利用膽固醇試劑盒,通過測(cè)量膽固醇吸光度檢測(cè)泡沫細(xì)胞內(nèi)膽固醇含量。2.ALDH2對(duì)泡沫細(xì)胞脂質(zhì)代謝的作用2.1 ALDH2對(duì)脂質(zhì)攝入相關(guān)受體的蛋白表達(dá)的影響Western Blot方法測(cè)量ox-LDL處理后ALDH2-、-與ALDH2+/+泡沫細(xì)胞主要的脂質(zhì)攝入受體CD36、LOX-1、SRA的蛋白表達(dá)變化。2.2 ALDH2對(duì)脂質(zhì)流出相關(guān)受體的蛋白表達(dá)的影響Western Blot方法測(cè)量Ox-LDL處理后ALDH2-/-與ALDH2+/+泡沫細(xì)胞主要的脂質(zhì)攝入受體ABCA1、ABCG1、ACAT-1的蛋白表達(dá)變化。3.ALDH2對(duì)CD36轉(zhuǎn)錄調(diào)控的作用的影響3.1 CD36在泡沫細(xì)胞形成中的作用ALDH2-/-與ALDH2+/+在ox-LDL處理前分別加入CD36受體抑制劑(Sulfo-N-succinimidyloleate,SSO),油紅O鏡下觀察泡沫細(xì)胞的形成并計(jì)數(shù)。3.2抑制CD36對(duì)泡沫細(xì)胞中脂質(zhì)的影響ALDH2-/-與ALDH2+/+在ox-LDL處理前分別加入CD36受體抑制劑(Sulfo-N-succinimidyloleate,SSO),利用膽固醇試劑盒,通過測(cè)量膽固醇吸光度檢測(cè)泡沫細(xì)胞內(nèi)膽固醇含量。3.3 ALDH2缺乏下CD36的mRNA變化Trizol 方法提取 ox-LDL 處理后 ALDH2-/-與ALDH2+/+的總 RNA,RT-PCR 方法檢測(cè)CD36 mRNA的水平。3.4 ALDH2影響CD36轉(zhuǎn)錄調(diào)控因子PPARyWestern Blot方法測(cè)量ox-LDL處理后ALDH2-/-與ALDH2+/+泡沫細(xì)胞中CD36的轉(zhuǎn)錄調(diào)控因子PPARy的蛋白水平。4.ALDH2對(duì)泡沫細(xì)胞凋亡的作用4.1 ALDH2對(duì)泡沫細(xì)胞凋亡的影響Tunel法觀察Ox-LDL處理后ALDH2/-與ALDH2+/+泡沫細(xì)胞凋亡情況,Western Blot方法檢測(cè)促凋亡蛋白Caspase-3的蛋白表達(dá)水平。4.2 ALDH2對(duì)毒性醛類物質(zhì)的影響利用丙二醛檢測(cè)試劑盒,通過測(cè)量丙二醛吸光度檢測(cè)泡沫細(xì)胞內(nèi)丙二醛含量。Western Blot方法檢測(cè)4-羥基壬烯醛對(duì)泡沫細(xì)胞內(nèi)全蛋白的加聚影響。4.3 ALDH2對(duì)泡沫細(xì)胞凋亡相關(guān)通路的影響Western Blot方法檢測(cè)調(diào)控凋亡的相關(guān)信號(hào)通路蛋白p-AKT/AKT、p-P38/P38 的變化。研究結(jié)果:1.ALDH2對(duì)乙醛脫氫酶2缺乏小鼠脂質(zhì)沉積的影響1.1 ALDH2基因缺乏增加動(dòng)脈粥樣硬化斑塊中的脂質(zhì)慢病毒干擾下乙醛脫氫酶2缺乏的APOE-/-組與正常APOE-/-組的主動(dòng)脈根部動(dòng)脈粥樣硬化斑塊脂質(zhì)沉積增加。1.2ALDH2影響泡沫細(xì)胞的形成1.2.1 ALDH2敲基因小鼠腹腔巨噬細(xì)胞的提取與鑒定免疫熒光顯示ALDH2-/-小鼠提取的原代腹腔細(xì)胞為ALDH2缺乏的巨噬細(xì)胞,ALDH2+/+小鼠提取的原代腹腔細(xì)胞正常表達(dá)ALDH2的巨噬細(xì)胞。1.2.2 ALDH2缺乏下抑制泡沫細(xì)胞形成ALDH2-/-組巨噬細(xì)胞與ALDH2+/+在氧化低密度脂蛋白刺激后都形成了泡沫細(xì)胞。其中ALDH2-/-泡沫細(xì)胞形成多于ALDH2+/+組。1.2.3 ALDH2缺乏的泡沫細(xì)胞內(nèi)脂質(zhì)沉積減少ALDH2-/-泡沫細(xì)胞中的膽固醇含量多于ALDH2+/+組。2.ALDH2對(duì)泡沫細(xì)胞脂質(zhì)代謝的影響2.1 ALDH2對(duì)脂質(zhì)攝入相關(guān)受體的蛋白表達(dá)Ox-LDL處理后,ALDH2-/-泡沫細(xì)胞與ALDH2+/+泡沫細(xì)胞相比,CD36蛋白表達(dá)量下降。LOX-1、SRA的蛋白表達(dá)無(wú)明顯變化。2.2 ALDH2對(duì)脂質(zhì)流出相關(guān)受體的蛋白表達(dá)Ox-LDL處理后,ALDH2-/-泡沫細(xì)胞與ALDH2+/+泡沫細(xì)胞相比,ABCA 1、ABCG1、ACAT-1蛋白表達(dá)無(wú)明顯變化。3.ALDH2對(duì)CD36轉(zhuǎn)錄調(diào)控的作用3.1 CD36在泡沫細(xì)胞形成中的作用加入CD36受體抑制劑后ALDH2-/-與ALDH2+/+泡沫細(xì)胞形成無(wú)明顯差異。3.2抑制CD36對(duì)泡沫細(xì)胞中脂質(zhì)的影響加入CD36受體抑制劑后ALDH2-/-與ALDH2+/+泡沫細(xì)胞內(nèi)膽固醇含量無(wú)明顯差異。3.3 ALDH2缺乏下CD36的mRNA變化Ox-LDL處理后,ALDH2-/-泡沫細(xì)胞與ALDH2+/+泡沫細(xì)胞相比,CD36 mRNA的表達(dá)水平下降。3.4 ALDH2影響CD36轉(zhuǎn)錄調(diào)控因子PPAR γOx-LDL處理后,ALDH2-/-泡沫細(xì)胞與ALDH2+/+泡沫細(xì)胞相比,CD36的轉(zhuǎn)錄調(diào)控因子PPARy的蛋白水平下降。4.ALDH2對(duì)泡沫細(xì)胞凋亡的作用4.1 ALDH2缺乏促進(jìn)泡沫細(xì)胞凋亡高濃度ox-LDL處理后ALDH2-/-與ALDH2+/+相比泡沫細(xì)胞發(fā)生更多的凋亡,促凋亡蛋白Caspase-3的蛋白表達(dá)水平上調(diào)。4.2 ALDH2缺乏下毒性醛類物質(zhì)增加高濃度ox-LDL處理后ALDH2-/-與ALDH2+/+相比泡沫細(xì)胞內(nèi)丙二醛含量增加,4-羥基壬烯醛對(duì)泡沫細(xì)胞內(nèi)全蛋白的加聚增多。4.3 ALDH2對(duì)泡沫細(xì)胞調(diào)亡相關(guān)通路的影響高濃度ox-LDL處理后ALDH2-/-與ALDH2+/+相比下,調(diào)控凋亡的信號(hào)通路蛋白p-AKT/AKT激活、調(diào)控增殖的信號(hào)通路蛋白p-P38/P38抑制。研究結(jié)論與意義1.首次發(fā)現(xiàn)ALDH2的缺乏促進(jìn)泡沫細(xì)胞內(nèi)毒性醛的增加,通過抑制脂質(zhì)攝取受體蛋白CD36的轉(zhuǎn)錄調(diào)控因子PPARγ下調(diào)CD36的蛋白表達(dá),從而減少泡沫細(xì)胞的脂質(zhì)攝取。2.首次揭示ALDH2缺乏的泡沫細(xì)胞激活凋亡信號(hào)通路p-AKT/AKT、抑制增殖信號(hào)通路p-P38/P38而引起泡沫細(xì)胞凋亡增加。
[Abstract]:Atherosclerosis is the primary cause of the disease in the heart, cerebrovascular and peripheral vascular diseases. Atherosclerosis is caused by many dangerous factors, such as hypertension, hyperlipidemia, smoking, diabetes and other dangerous factors, and its pathophysiological process is complicated. Lipid metabolism disorders and disorders are recognized as the pathological basis of atherosclerosis. In the process of initial atherosclerosis, lipids are deposited on the wall of the blood vessel, and macrophages raise and enter the endothelium to devour the lipid, thus differentiating into foam cells and forming lipid stripes in early atherosclerotic plaques. In the late stage of atherosclerosis, the necrosis or apoptosis of foam cells causes lipid release. It forms the core of necrosis and increases the instability of plaque. Therefore, the occurrence and development of the foam cells run through the pathophysiological process of atherosclerosis. Acetaldehyde dehydrogenase 2 (Aldehyde dehydrogenase 2, ALDH2) is an aldehyde metabolizing enzyme located on the mitochondria. The activity of the wild type ALDH2 enzyme is high and the mutant ALDH2 enzyme activity is reduced. In recent years, epidemiological studies have shown that ALDH2 is involved in acute arterial syndrome and coronary atherosclerotic heart disease. Several studies from Japan, China and South Korea have proved that ALDH2 mutants are closely related to cardiovascular diseases such as myocardial infarction and acute coronary syndrome. In 2012, a whole genome association analysis of AL DH2 gene polymorphism and coronary heart disease have been studied, which confirmed that the population of mutant ALDH2 has high incidence of coronary syndrome and coronary atherosclerotic disease. Previous studies have shown that ALDH2 plays an important role in the protection of endothelial cells and myocardial cells, but the role of ALDH2 in foam cells has not been reported. In the early study of the group, we found that mice using lentivirus knockout ALDH2 showed more carotid atherosclerotic plaques in which the lipid deposition was significantly increased. In this experiment, we also confirmed that ALDH2 knockout mice also showed more lipid deposition at the root of the aorta. Because the foam cells were atherosclerosis. There is an essential part of lipid deposition in plaque. At the same time, ALDH2 research has shown that it plays an important role in the cardiovascular system in recent years. So we assume that ALDH2 plays an important role in foamy cells and is related to the laboratory test in vivo and in vitro. Objective 1. to study ALDH2 for arterial porridge. The effect of sclerosing lipid deposition on the mechanism of ALDH2 in the regulation of lipid deposition in foam cells to provide further theoretical support for the pathophysiological process of atherosclerosis. Methods 1. acetaldehyde dehydrogenase 2 deficiency mice lipid deposition changes 1.1 ALDH2 genes lack of increased lipid ApoE-/- in atherosclerotic plaques Rats were fed by high fat feeding to construct the atherosclerotic model, using lentivirus to interfere with the expression of ALDH2 in mice. The rats were randomly divided into ALDH2 deficiency experimental group and normal ALDH2 control group. The atherosclerotic plaque of the aortic root of mice was made into frozen section, and the lipid content of.1.2ALDH2 was used to detect the effect of.1.2ALDH2 on the shape of the foam cells. Extraction and identification of peritoneal macrophages of 1.2.1 ALDH2 knockout mouse peritoneal macrophages, ALDH2 knockout mice and wild mice were used as macrophage donors and mouse peritoneal macrophages were extracted under thioglycollate stimulation. The expression of peritoneal macrophages and ALDH2 was identified by cell immunofluorescence method.1.2.2 ALDH2 deficiency on foams The primary macrophages of mice were divided into ALDH2 deficiency group (ALDH2-/-) and control group (ALDH2+/+). After addition of oxidized low density lipoprotein (LDL), lipid staining was carried out with oil red O. The effect of.1.2.3 ALDH2 deficiency on the lipid deposition of foam cell in the foam cells was observed under the microscope, and the primary macrophage of the mouse was added to the foam cell. After oxidation of low density lipoprotein (LDL), use Cholesterol Reagent box to measure the effect of cholesterol content.2.ALDH2 on the lipid metabolism of foam cells by measuring cholesterol absorbency. Effect of 2.1 ALDH2 on the protein expression of lipid intake related receptors by Western Blot method, ALDH2-, and ALDH2+/+ foam cells after ox-LDL treatment Major lipid intake receptor CD36, LOX-1, SRA protein expression changes,.2.2 ALDH2 effect on the protein expression of lipid efflux receptor, Western Blot method measured the main lipid intake receptor ABCA1 of ALDH2-/- and ALDH2+/+ foam cells after Ox-LDL treatment and the effect of protein expression changes on the regulation of transcription. The effect of 3.1 CD36 on the formation of foam cells ALDH2-/- and ALDH2+/+ were added to the CD36 receptor inhibitor (Sulfo-N-succinimidyloleate, SSO) before ox-LDL treatment. The formation of foam cells was observed under the oil red O microscope and the effect of.3.2 inhibition CD36 on the lipid in the foam cells was counted. Receptor inhibitor (Sulfo-N-succinimidyloleate, SSO), using Cholesterol Reagent box, the total RNA of ALDH2-/- and ALDH2+/+ after ox-LDL treatment was extracted by measuring the cholesterol content of.3.3 ALDH2 in foam cells by the measurement of cholesterol absorbency and the mRNA change Trizol method under the absence of CD36. The effect of transcription regulator PPARyWestern Blot on ALDH2-/- and ALDH2+/+ in ALDH2-/- and ALDH2+/+ foam cells the effect of protein level.4.ALDH2 on the apoptosis of foam cells 4.1 ALDH2 on the apoptosis of foam cells, the Tunel method was used to observe the apoptosis of ALDH2/- and foam cells after Ox-LDL treatment. Lot method was used to detect the protein expression level of apoptotic protein Caspase-3.4.2 ALDH2 on the toxicity of toxic aldehydes using malondialdehyde detection kit. By measuring malondialdehyde absorbance detection of malondialdehyde content in foam cells,.Western Blot method was used to detect the effect of 4- hydroxyl nonylaldehyde on the accumulation of whole protein in the foam cell by the addition of 4- hydroxyl nonylaldehyde to.4.3 ALDH2 pair of bubbles. Influence of Western Blot method on apoptosis related signaling pathway protein p-AKT/AKT and p-P38/P38 changes. Results: the effect of 1.ALDH2 on lipid deposition in acetaldehyde dehydrogenase 2 deficiency in mice; 1.1 ALDH2 gene deficiency increased glyaldehyde dehydrogenase 2 in atherosclerotic plaques Lipid deposition in atherosclerotic atherosclerotic plaques in the aortic root of the APOE-/- group and the normal APOE-/- group increased the effect of.1.2ALDH2 on the formation of the foam cells. The extraction and identification of the peritoneal macrophages in the 1.2.1 ALDH2 knockout mice, the immunofluorescence showed that the primary peritoneal cells extracted by ALDH2-/- mice were ALDH2 deficient macrophages, ALDH2+/+ mice The extracted primary peritoneal cells normally express ALDH2 macrophage.1.2.2 ALDH2 deficiency to inhibit the formation of foam cells and form ALDH2-/- group macrophages and ALDH2+/+ to form foam cells after oxidative low density lipoprotein stimulation. Among them, ALDH2-/- foam cells form more than the ALDH2+/+ group.1.2.3 ALDH2 deficient foam cells in the lipid deposition. The cholesterol content in the small ALDH2-/- foam cells was more than that of the ALDH2+/+ group.2.ALDH2 on the lipid metabolism of the foam cells. 2.1 ALDH2 was treated with the protein expression of the receptor related to the lipid intake. The ALDH2-/- foam cells were compared with the ALDH2+/+ foam cells, the expression of CD36 protein decreased.LOX-1, and the protein expression of SRA had no obvious change of.2.2 ALDH2. After Ox-LDL treatment of the protein expression of the lipid outflow related receptor, ALDH2-/- foam cells compared with ALDH2+/+ foam cells, ABCA 1, ABCG1, ACAT-1 protein expression did not significantly change the role of.3.ALDH2 on the regulation of CD36 transcriptional regulation. 3.1 CD36 in the formation of foam cells added to the CD36 receptor inhibitor, ALDH2-/- and ALDH2+/+ foam cells were formed. Significant difference in the effect of.3.2 on the effect of CD36 on the lipid in the foam cells. There is no significant difference in the cholesterol content between the ALDH2-/- and the ALDH2+/+ foam cells after the CD36 receptor inhibitor..3.3 ALDH2 lack of CD36's mRNA change Ox-LDL treatment, ALDH2-/- foam cells compared with the ALDH2+/+ foam cells CD36 transcriptional regulator PPAR gamma Ox-LDL treatment, ALDH2-/- foam cells compared with ALDH2+/+ foam cells, CD36 transcriptional regulator PPARy protein level decreased.4.ALDH2 to the apoptosis of foam cells 4.1 ALDH2 deficiency promoted the foam cell apoptosis high concentration ox-LDL processing, ALDH2-/- compared with ALDH2+/+ cells compared to ALDH2+/+ cells. Apoptosis, protein expression level of apoptotic protein Caspase-3 up regulate the increase of the content of malondialdehyde in foam cells after ALDH2-/- and ALDH2+/+, and the effect of 4- hydroxyl nonylaldehyde on the apoptosis of foam cells after.4.2 ALDH2 deficiency increases the concentration of ALDH2-/- and ALDH2+/+. The effect of 4- hydroxyl nonylaldehyde on the apoptosis of foam cells in foam cells After high concentration of ox-LDL, ALDH2-/- and ALDH2+/+ are compared with ALDH2+/+, the signaling pathway protein p-AKT/AKT regulates apoptosis and regulates the proliferation of signaling pathway protein p-P38/P38. Conclusion and significance 1. first found that the deficiency of ALDH2 promotes the increase of toxic aldehyde in foam cells and inhibits the transcriptional regulation of the lipid uptake receptor protein CD36. SubPPAR gamma down regulated the protein expression of CD36, thus reducing the lipid uptake by.2. in foam cells for the first time to reveal the p-AKT/AKT of the apoptotic signaling pathway in the ALDH2 deficient foam cells, and to inhibit the proliferation signal pathway p-P38/P38 and increase the apoptosis of the foam cells.
【學(xué)位授予單位】：山東大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R543.5

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