發(fā)布時間：2018-05-20 06:17

  本文選題：Omentin-1 + 丹參酮IIA��； 參考：《南華大學》2016年博士論文

【摘要】：動脈粥樣硬化(Atherosclerosis,As)在全球的罹患率以及致死率都名居前列,嚴重危害人類的健康。在動脈粥樣硬化早期,其標志性病理特征是血管內皮下大量的巨噬細胞內脂質蓄積以及泡沫細胞的形成。泡沫細胞最終壞死崩解,釋放出細胞內的膽固醇,是構成動脈粥樣硬化斑塊的最主要成分,促進動脈粥樣硬化的進一步進展。因此,促進巨噬細胞內膽固醇流出及體內膽固醇逆向轉運(reverse cholesterol transport,RCT),從而抑制泡沫細胞形成和血管壁內脂質沉積,對動脈粥樣硬化性的防治具有重要意義。三磷酸腺苷結合盒轉運體A1(ATP binding cassette transporter A1,ABCA1)是一個膜整合蛋白,其以ATP作為能源將胞內游離的膽固醇及磷脂轉運至胞膜的外側面,最終與貼附在細胞表面的載脂蛋白AI(apoprotein AI,apoAI)結合,從而形成新生的高密度脂蛋白(high density lipoprotein,HDL)。這是HDL生成所必需的過程,也是促進巨噬細胞內過多的膽固醇外流以及rct的關鍵步驟。abca1在巨噬細胞中的表達以及其活性往往受到轉錄及轉錄后水平的精細調控。網(wǎng)膜素(omentin)是一類新發(fā)現(xiàn)的脂肪細胞因子,主要由網(wǎng)膜脂肪組織表達和釋放。值得注意的是,研究發(fā)現(xiàn)這種基因可調節(jié)葡萄糖攝取。肥胖或肥胖相關疾病患者,包括2型糖尿病、內皮功能障礙、頸動脈粥樣硬化和冠狀動脈疾病,發(fā)現(xiàn)其血漿omentin-1水平降低了。研究證明,omentin-1與高密度脂蛋白膽固醇(hdl-c)呈正相關,與葡萄糖和甘油三酸酯水平呈負相關。代謝綜合征(mets)初期患者循環(huán)omentin-1水平異常者其罹患糖尿病和心血管疾病的風險更高。因此,omentin-1與代謝綜合征密切相關,在代謝綜合征患者的動脈粥樣硬化發(fā)生發(fā)展中產生重要作用。omentin-1在rct、脂質代謝和as中差異表達的發(fā)現(xiàn)為我們提供了新的途徑和視角。因此,omentin-1有望成為心血管保護因子和干預靶點之一。然而,omentin-1在abca1表達及導致提高hdl功能和膽固醇逆向轉運中的作用研究尚少。本研究中,我們研究omentin-1對巨噬細胞abca1表達的作用和潛在的分子機制。為了探討omentin-1抗動脈粥樣硬化的相關作用機制,我們首先在第一部分實驗中觀察omentin-1對thp-1巨噬細胞abca1表達、胞內膽固醇流出和脂質含量的影響。在第二部分實驗中我們探索了omentin-1介導thp-1巨噬細胞abca1表達及膽固醇流出的作用機制。接著,我們在第三部分實驗中,觀察了omentin-1對apoe-/-小鼠的血脂水平、膽固醇逆向轉運和動脈粥樣硬化病變的影響。最后,我們在第四部分實驗中,觀察了具有較強調脂作用的丹參酮iia(tanshinoneiia,tan)對巨噬細胞的omentin-1和abca1的表達、脂質代謝,以及對apoe-/-小鼠的動脈粥樣硬化病變的影響,研究tan通過上調omentin-1發(fā)揮抗動脈粥樣硬化的作用機制。本研究揭示了omentin-1抗動脈粥樣硬化的作用以及機制,也許為動脈粥樣硬化性疾病提供新的防治靶點。第1章omentin-1對thp-1巨噬細胞abca1表達及膽固醇流出的影響目的:觀察omentin-1對thp-1巨噬細胞abca1mrna及蛋白表達水平、胞內膽固醇流出和脂質含量的影響。方法:用omentin-1和/或lxrαsirna處理thp-1源性巨噬細胞后,用rt-pcr方法檢測各個實驗組細胞的abca1mrna的表達,westernblot檢測abca1蛋白水平,hplc檢測胞內總膽固醇(tc)游離膽固醇(fc)及膽固醇酯(ce)含量,液體閃爍計數(shù)儀檢測胞內膽固醇流出,油紅o染色觀察胞內脂滴情況。結果:omentin-1呈時間和濃度依賴性上調巨噬細胞abca1的表達,促進胞內膽固醇流出,降低胞內tc、fc和ce含量,抑制胞內脂質蓄積和泡沫細胞形成。而abca1sirna與omentin-1共處理細胞后,明顯抑制omentin-1促膽固醇流出的作用,胞內脂質蓄積和泡沫細胞形成明顯加劇。結論:(1)omentin-1增加thp-1巨噬細胞abca1mrna和蛋白表達。(2)omentin-1促進abca1介導的thp-1巨噬細胞脂質流出,抑制巨噬細胞內脂質蓄積和泡沫細胞形成。第2章omentin-1介導thp-1巨噬細胞abca1表達及膽固醇流出的作用機制目的:探索omentin-1介導thp-1巨噬細胞abca1表達及膽固醇流出的作用機制。方法:分別用omentin-1或和lxrαsirna、pi3ksirna、aktsirna、pi3k抑制劑ly2940029及akt抑制劑himo處理thp-1源性巨噬細胞24h后,westernblot檢測abca1lxrα蛋白水平,hplc檢測胞內總膽固醇(tc)游離膽固醇(fc)及膽固醇酯(ce)含量,液體閃爍計數(shù)儀檢測胞內膽固醇流出,油紅o染色觀察胞內脂滴情況。結果:omentin-1上調巨噬細胞abca1的表達,促進胞內膽固醇流出,降低胞內tc、fc和ce含量,抑制胞內脂質蓄積和泡沫細胞形成。而分別加用lxrαsirna、pi3ksirna、aktsirna、pi3k抑制劑ly2940029及akt抑制劑himo與omentin-1共處理細胞后,明顯抑制abca1的表達及其促膽固醇流出的作用,胞內脂質蓄積和泡沫細胞形成明顯加劇。結論:(1)omentin-1通過pi3k/akt途徑增加人thp-1巨噬細胞lxrα和abca1表達,促進脂質流出,抑制巨噬細胞內脂質蓄積和泡沫細胞形成。第3章omentin-1對apoe-/-小鼠動脈粥樣硬化的影響目的:探討omentin-1對apoe-/-小鼠體內rct、血脂水平、主動脈壁的脂質沉積,以及對粥樣硬化病變的影響和機制。方法:采用高脂飲食(含15%豬油+0.25%膽固醇)喂飼的45只apoe-/-小鼠,并隨機地分為三組,分別為:高脂對照組、omentin-1組、omentin-1+ly2940029組。omentin-1組腺病毒轉染omentin-1以1×108pfu/kg(pfu:空斑形成單位),ome+ly組小鼠再加以20mg/kgpi3k抑制劑ly2940029,溶入0.2ml的生理鹽水中進行尾靜脈注射,每2周注射一次,都用基礎飲食加上高脂高膽固醇(15%豬油+0.25%膽固醇)喂養(yǎng),直至實驗結束,共處理8周。采用液體閃爍計數(shù)以測定mpm來源的rct效率;采用酶氧化法檢測甘油三酯(tg)、總膽固醇、高密度脂蛋白膽固醇(hdl-c)及低密度脂蛋白膽固醇(ldl-c)等血脂水平;采用蘇丹Ⅳ染色以顯示主動脈內膜的as病變情況;采用he染色顯示主動脈竇的as病變情況;采用油紅o染色以觀察主動脈竇處脂質沉積的情況;采用masson三色染色以顯示斑塊中的膠原纖維;采用westernblot檢測小鼠的主動脈abca1等蛋白的表達。結果:輸注了轉染omentin-1的質粒明顯增強了apoe-/-小鼠糞便中3h固醇的放射活性,并增高血漿的hdl-c水平,降低了ldl-c水平,使主動脈內膜的as病變面積減小,減少主動脈竇處的脂質沉積,增強as斑塊的穩(wěn)定性,增加了主動脈abca1的蛋白表達。注射ly2940029則明顯減少糞便中的固醇水平,增加主動脈壁內脂質沉積,促進動脈粥樣硬化病變的發(fā)展,下調abca1蛋白表達。結論:(1)omentin-1促進apoe-/-鼠體內rct和升高血漿hdl-c水平。(2)omentin-1抑制apoe-/-鼠主動脈脂質沉積,延緩粥樣硬化病變的進展。(3)omentin-1增強apoe-/-鼠主動脈壁組織的abca1表達,并且其可能是通過pi3k/akt信號通路而起調節(jié)作用的。第4章丹參酮iia對巨噬細胞omentin-1/abca1水平及apoe-/-小鼠主動脈病變的影響及其機制目的:觀察丹參酮iia(tanshinoneiia,tan)對thp-1巨噬細胞中omentin-1和abca1表達,以及對apoe-/-小鼠體內血脂水平、rct、主動脈壁as病變的影響,并探討tan抗as的作用機制。方法:用tan處理thp-1巨噬細胞,并結合omentin-1sirna轉染thp-1巨噬細胞后,采用實時熒光定量pcr以檢測omentin-1和abca1水平,采用westernblot檢測omentin-1和abca1蛋白表達;采用液體閃爍計數(shù)以測定荷脂THP-1巨噬細胞內的膽固醇流出情況,采用HPLC檢測細胞內脂質的含量。高脂飲食(含15%豬油+0.25%膽固醇)喂飼的45只apoE-/-小鼠被隨機分為三組,分別為:高脂對照組、丹參酮IIA組和丹參酮IIA+Omentin-1 siRNA組。采用液體閃爍計數(shù)以測定MPM來源的RCT效率,采用酶氧化法以檢測TG、TC、HDL-c和LDL-c等的血脂水平,采用蘇丹Ⅳ染色以顯示主動脈內膜的As病變情況,采用HE染色以顯示主動脈竇As病變情況,采用油紅O染色以顯示主動脈竇處脂質的沉積情況,采用Masson三色染色以顯示As斑塊中的膠原纖維情況。結果:觀察到Tan可以呈劑量和時間依賴性地增強了THP-1巨噬細胞中Omentin-1和ABCA1蛋白的表達,增強細胞內膽固醇流出,并減少細胞內的FC、CE和TC含量。Tan可增強apoE-/-小鼠糞便中3H膽固醇的放射活性,并增高血漿HDL-c水平,降低LDL-c水平,增強主動脈Omentin-1和ABCA1表達,減少了主動脈內膜的As變面積,減輕了主動脈竇處的脂質沉積,增強了斑塊的穩(wěn)定性。抑制Omentin-1表達后,則明顯削弱Tan的上述作用。結論:(1)Tan抗As的作用與增強巨噬細胞內膽固醇外流和體內的RCT功能密切相關。(2)Tan抗As的作用機制與升高Omentin-1水平并進而增加ABCA1表達有關,并且可能是通過PI3K/Akt信號通路而起調節(jié)作用的。
[Abstract]:Atherosclerosis (As) is in the forefront of the global morbidity and mortality rate, which seriously endangers human health. In the early stage of atherosclerosis, its marked pathological feature was the accumulation of lipid and the formation of foam cells in a large number of macrophages under vascular endothelium. Internal cholesterol, the most important component of atherosclerotic plaques, promotes the further progress of atherosclerosis. Therefore, it promotes cholesterol outflow in macrophages and reverse cholesterol transport (RCT) in vivo, which inhibits the formation of foamy cells and the lipid deposition in the blood vessel wall. Adenosine triphosphate binding cassette transporter A1 (ATP binding cassette transporter A1, ABCA1) is a membrane integrin that transships intracellular free cholesterol and phospholipids to the outer side of the cell membrane with ATP as a source of energy and eventually combines with the apolipoprotein AI (apoprotein AI, apoAI) attached to the surface of the cell. The formation of high density lipoprotein (HDL), which is a necessary process for HDL production, is also a key step in promoting excessive cholesterol Exodus in macrophages and the key step in RCT, the expression of.Abca1 in macrophages and its activity often finely regulated by the transcriptional and post transcriptional levels. The omentin (omentin) is a HDL. A newly discovered class of adipocyte factors, mainly expressed and released from omentum adipose tissue. It is worth noting that this gene has been found to regulate glucose uptake. Patients with obesity or obesity related diseases, including type 2 diabetes, endothelial dysfunction, carotid atherosclerosis, and coronary artery disease, have been found to be in the plasma omentin-1 level. Lower. Studies have shown that omentin-1 is positively related to high density lipoprotein cholesterol (HDL-C) and is negatively correlated with glucose and triglyceride levels. Patients with abnormal circulating omentin-1 levels in the early stage of metabolic syndrome (MetS) have a higher risk of developing diabetes and cardiovascular disease. Therefore, omentin-1 is closely related to metabolic syndrome, in metabolism. The discovery of.Omentin-1 in the occurrence and development of atherosclerosis in patients with RCT, the discovery of differential expression in lipid metabolism and as provides us with new ways and perspectives. Therefore, omentin-1 is expected to become one of the cardiovascular protective factors and intervention targets. However, omentin-1 is expressed in ABCA1 and leads to the improvement of HDL function and bile. In this study, we studied the role of omentin-1 on the expression of ABCA1 in macrophages and the potential molecular mechanism in this study. In order to explore the mechanism of omentin-1 anti atherosclerosis, we first observed the expression of ABCA1 and intracellular cholesterol in THP-1 macrophages in the first part of the experiment. The effect of outflow and lipid content. In the second experiment, we explored the mechanism of omentin-1 mediated THP-1 macrophage ABCA1 expression and cholesterol efflux. Then, in the third experiment, we observed the effects of omentin-1 on blood lipid levels, cholesterol reverse transport and atherosclerotic lesions in apoe-/- mice. In the fourth experiment, we observed the expression of omentin-1 and ABCA1 in macrophages, lipid metabolism, and the effect on atherosclerotic lesions of apoe-/- mice, which had strong lipid regulating effect, and studied the mechanism of the anti atherosclerosis mechanism of Tan by up regulation of omentin-1. This study was to study the mechanism of the anti atherosclerosis of Tan by up regulation of omentin-1. The anti atherosclerotic effect and mechanism of omentin-1 may provide new prevention and treatment targets for atherosclerotic disease. First the effect of omentin-1 on ABCA1 expression and cholesterol efflux of THP-1 macrophages is to observe the expression level of abca1mrna and protein in THP-1 macrophages, intracellular cholesterol efflux and lipids. Methods: after the treatment of THP-1 derived macrophages with omentin-1 and / or LXR alpha siRNA, the expression of abca1mrna in the cells of each experimental group was detected by RT-PCR, the level of ABCA1 protein was detected by Westernblot, and the content of intracellular total cholesterol (TC) free cholesterol (FC) and cholesteryl ester (CE) was detected by HPLC, and the liquid scintillation counting instrument was used to detect the internal gallbladder. Results: omentin-1 showed time and concentration dependent increase of ABCA1 expression in macrophages, promoted intracellular cholesterol efflux, reduced intracellular TC, FC and Ce content, inhibited intracellular lipid accumulation and foam cell formation, while abca1sirna and omentin-1 co treated cells significantly inhibited omentin-1 promoted by abca1sirna and omentin-1. The effect of cholesterol outflow, intracellular lipid accumulation and foam cell formation increased obviously. Conclusion: (1) omentin-1 increases the abca1mrna and protein expression of THP-1 macrophages. (2) omentin-1 promotes lipid efflux of ABCA1 mediated THP-1 macrophages and inhibits lipid accumulation and foam cell formation in macrophages. Second chapter omentin-1 mediates THP-1 meagage The mechanism of the action mechanism of ABCA1 expression and cholesterol efflux: To explore the mechanism of omentin-1 mediated ABCA1 expression and cholesterol efflux in THP-1 macrophages. Methods: omentin-1 or LXR alpha siRNA, pi3ksirna, aktsirna, PI3K inhibitor ly2940029 and Akt inhibitors were used to detect the derived macrophages. R alpha protein level, HPLC detection of intracellular total cholesterol (TC) free cholesterol (FC) and cholesteryl ester (CE) content, liquid scintillation counting apparatus to detect intracellular cholesterol efflux, oil red O staining to observe the intracellular lipid droplets. Results: omentin-1 increases the expression of ABCA1 in macrophages, promotes intracellular cholesterol efflux, reduces intracellular TC, FC and Ce content, inhibits intracellular. Lipid accumulation and foam cell formation. After adding LXR alpha siRNA, pi3ksirna, aktsirna, PI3K inhibitor ly2940029 and Akt inhibitor HimO and omentin-1 co processing cells, the expression of ABCA1 and the effect of cholesterol efflux were inhibited, and the accumulation of intracellular lipids and the formation of foam cells were obviously intensified. Conclusion: (1) omentin-1 through pi3k/akt. Diameter increases the expression of LXR alpha and ABCA1 in human THP-1 macrophages, promotes lipid outflow, inhibits lipid accumulation in macrophages and foams cell formation. Third the effects of omentin-1 on atherosclerosis in apoe-/- mice: the study of omentin-1 on RCT, lipid levels, lipid deposition in the aortic wall and atherosclerosis in apoe-/- mice Methods: 45 apoe-/- mice fed with high fat diet (containing 15% lard +0.25% cholesterol) were randomly divided into three groups: high fat control group, omentin-1 group, omentin-1+ly2940029 group.Omentin-1 adenovirus transfected omentin-1 with 1 x 108pfu/kg (pfu: empty plaque formation unit), ome+ly group mice then 20mg/kgpi3k The inhibitor ly2940029, injected into the normal saline of 0.2ml, injected the tail vein every 2 weeks, fed the basal diet plus high fat and high cholesterol (15% lard +0.25% cholesterol), until the end of the experiment, for 8 weeks. The liquid scintillation counting was used to determine the RCT efficiency of the MPM source, and the enzyme oxidation method was used to detect triglyceride (TG), general Cholesterol, high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) and other blood lipid levels; Sultan IV staining was used to show the as lesion of the aortic intima; he staining was used to display the as lesion of the aortic sinus, and the oil red O staining was used to observe the lipid deposition in the aortic sinus; Masson trichromatic staining was used. The expression of ABCA1 and other proteins in the aorta of the mice was detected by Westernblot. Results: the transfection of omentin-1 transfected plasmid significantly enhanced the radioactivity of 3H sterol in the feces of apoe-/- mice, increased the level of HDL-C in plasma, reduced the LDL-C level, reduced the as lesion area of the aorta intima, and reduced the lesion area of the aorta intima. The lipid deposition at the sinus of aortic sinus enhanced the stability of as plaque and increased the protein expression of ABCA1 in the aorta. Injection of ly2940029 significantly reduced the level of sterol in the feces, increased the lipid deposition in the aortic wall, promoted the development of atherosclerotic lesions, and lowered the expression of ABCA1 protein. Conclusion: (1) omentin-1 promotes RCT in the body of apoe-/- mice. Increase the plasma HDL-C level. (2) omentin-1 inhibits the aortic lipid deposition in apoe-/- rats and delays the progression of atherosclerotic lesions. (3) ABCA1 expression in the aorta wall of apoe-/- rats is enhanced by omentin-1, and it may be regulated by the pi3k/akt signaling pathway. The fourth chapter of tanshinone IIA to macrophage omentin-1/abca1 level and apoe-/ Effect and mechanism of mouse aortic disease: To observe the expression of tanshinone IIA (tanshinoneIIA, tan) on omentin-1 and ABCA1 in THP-1 macrophages, as well as the effect on serum lipid level, RCT, as lesion of the aortic wall in apoe-/- mice, and to explore the mechanism of Tan as on tan. After transfection of RNA to THP-1 macrophages, real-time fluorescence quantitative PCR was used to detect the level of omentin-1 and ABCA1. The expression of omentin-1 and ABCA1 protein was detected by Westernblot; liquid scintillation counting was used to determine the cholesterol efflux in the lipid THP-1 macrophages. The content of intracellular lipids was detected by HPLC. High fat diet (containing 15% lard +0.25%) was used. 45 apoE-/- mice fed with cholesterol were randomly divided into three groups: the high fat control group, the tanshinone IIA group and the tanshinone IIA+Omentin-1 siRNA group. The liquid scintillation counting was used to determine the RCT efficiency of the MPM source. The lipid levels of TG, TC, HDL-c and LDL-c were detected by enzyme oxidation, and the Sultan IV staining was used to display the internal aorta. The As lesion of the membrane was used to display the As lesion of the aortic sinus by HE staining. The oil red O staining was used to show the deposition of lipid in the aortic sinus, and the Masson stain was used to show the collagen fiber in the As plaque. The results showed that Tan could be dosed and time dependent on the increase of Omentin-1 and A in THP-1 macrophages. The expression of BCA1 protein, the increase of intracellular cholesterol efflux, and the reduction of the intracellular FC, CE and TC content.Tan can enhance the radioactivity of 3H cholesterol in the apoE-/- mice, increase the level of HDL-c, reduce the LDL-c level, increase the expression of Omentin-1 and ABCA1 in the aorta, reduce the area of the intima intima of the aorta, and reduce the sinus of the aortic sinus. Lipid deposition enhanced the stability of plaque. After inhibiting the expression of Omentin-1, the effect of Tan was obviously weakened. Conclusion: (1) the anti As effect of Tan is closely related to the enhancement of cholesterol Exodus in macrophages and the function of RCT in the body. (2) the mechanism of the anti As action of Tan is related to the increase of Omentin-1 level and the increase of ABCA1 expression, and may be associated with As. It is regulated by the PI3K/Akt signaling pathway.
【學位授予單位】：南華大學
【學位級別】：博士
【學位授予年份】：2016
【分類號】：R543.5

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