本文選題：低氧預(yù)處理 + 脂肪間充質(zhì)干細(xì)胞　； 參考：《中國人民解放軍醫(yī)學(xué)院》2016年博士論文

【摘要】：[背景]心肌梗死是嚴(yán)重威脅人類健康的疾病。我國每年約有2.9億人罹患心血管疾病,并有350萬人因此而喪生。心血管疾病死亡率位居我國城鄉(xiāng)居民總死亡原因的首位,且呈逐年攀升趨勢。目前心肌梗死的主要治療手段還是藥物和手術(shù),雖然它們能夠促進(jìn)血管再通,減輕心肌的持續(xù)性損傷,但二者對梗死的心肌組織并無再生作用,且不能有效逆轉(zhuǎn)心肌梗死后的纖維化。干細(xì)胞移植是一種新興的治療方法,其目的是促進(jìn)缺血區(qū)心肌和血管生成,減少心肌細(xì)胞凋亡,減輕心室重塑。脂肪間充質(zhì)干細(xì)胞(Adipose-derived mesenchymal stem cells,ASC)以其獨特的優(yōu)勢,逐漸成為當(dāng)前研究的熱點。雖然ASC的安全性和有效性已得到初步認(rèn)識,但其在體內(nèi)的存活和顯效還受到多個環(huán)節(jié)的影響。為了提高干細(xì)胞在局部的存活效率,研究者們開始對干細(xì)胞進(jìn)行體外預(yù)處理或者對組織微環(huán)境進(jìn)行改善,以利于細(xì)胞的長期存活和發(fā)揮修復(fù)功能。低氧預(yù)處理(Hypoxia precondition,HP)是增加干細(xì)胞存活率的簡單有效的方法。為了適應(yīng)移植后在梗死區(qū)局部的低氧環(huán)境,在體外對ASC進(jìn)行低氧培養(yǎng),以此增強細(xì)胞對低氧的耐受性和抗凋亡能力,同時促進(jìn)其分泌多種生長因子,有利于細(xì)胞進(jìn)入體內(nèi)后發(fā)揮修復(fù)和再生功能。臍血單核細(xì)胞(Cord blood mononuclear cells,CBMNCs)能夠促進(jìn)血管新生和血管內(nèi)皮化,改善梗死局部的微循環(huán)。內(nèi)皮細(xì)胞的再血管化可以為移植的干細(xì)胞帶來營養(yǎng)和氧氣,有利于干細(xì)胞在局部的存活。因此,將體外預(yù)處理與體內(nèi)微環(huán)境的改善結(jié)合起來,可能更有利于細(xì)胞在局部的長期存活。[目的]1.研究ASC的培養(yǎng),鑒定和體外誘導(dǎo)分化能力；以及CBMNCs分離和凍存?zhèn)溆茫?.檢測低氧預(yù)處理前后ASC的基因表達(dá)變化；并體外模擬心梗環(huán)境培養(yǎng)HP-ASC和ASC,比較二者基因表達(dá)水平的變化；3.評價HP-ASC治療大鼠心肌梗死是否優(yōu)于ASC；4.評價HP-ASC聯(lián)合CBMNCs治療大鼠心肌梗死是否優(yōu)于單一細(xì)胞移植效果。[方法]1.以健康成人脂肪抽吸術(shù)后的脂肪組織為實驗對象,用膠原酶消化分解后,離心取下層SVF細(xì)胞,接種培養(yǎng)。用MTT法測量細(xì)胞密度并繪制ASC生長曲線；流式細(xì)胞術(shù)檢測ASC細(xì)胞表面標(biāo)記；分別以成骨、成脂、成軟骨誘導(dǎo)液誘導(dǎo)ASC分化,利用組織化學(xué)染色和免疫蛆化染色檢測其多向分化潛能。來自健康嬰兒的臍血離心沉降法分離出CBMNCs,檢測細(xì)胞數(shù)量及活性細(xì)胞比例,凍存?zhèn)溆谩?.ASC在低氧(2%O2)條件下培養(yǎng)24h,提取細(xì)胞RNA,比較HP-ASC與未處理ASC基因表達(dá)情況；模擬體內(nèi)心梗局部微環(huán)境,取大鼠心梗后3d的心臟組織,研磨成漿,加入血清及必須氨基酸等配制成心�；旌弦骸P-ASC和ASC在此混合液中培養(yǎng)5d,檢測細(xì)胞在微環(huán)境誘導(dǎo)下基因表達(dá)的變化；3.兩月齡Wistar雌性大鼠30只,按照隨機數(shù)法將實驗動物隨機分為3組,HP-ASC組,ASC組和PBS組,每組各10只大鼠。結(jié)扎冠狀動脈左前降支建立心肌梗死損傷模型,動物心梗后即刻心肌內(nèi)注射干細(xì)胞(總量：2×106)或PBS。細(xì)胞移植后7d和15d每組分別處死5只大鼠,收集心臟組織,制作冰凍組織切片和石蠟組織切片。比較各組之間心梗部位的大體形態(tài)學(xué)變化,心梗區(qū)占左心室比例,細(xì)胞移植效率,細(xì)胞凋亡數(shù)量和新生血管密度。4. 兩月齡Wistar雌性大鼠60只,按照隨機數(shù)法將實驗動物隨機分為4組,HP-ASC組,HP-ASC+CBMNCs組,CBMNCs組和PBS組,每組各15只大鼠。模型成功后即刻進(jìn)行細(xì)胞移植,細(xì)胞總量為2×106(聯(lián)合組細(xì)胞比例1：1)。每組動物分別在手術(shù)后7d,15d和30d各取5只處死。比較各組之間心梗部位的大體形態(tài)學(xué)變化,心梗區(qū)占左心室比例和室壁厚度,細(xì)胞移植存活率和新生血管密度。[結(jié)果]1.原代ASC接種6h后,部分細(xì)胞開始貼壁生長,24-48h后細(xì)胞開始出現(xiàn)集落樣增長(CFU)。第3代以后,細(xì)胞呈典型纖維母細(xì)胞樣梭形外觀,開始呈漩渦狀生長,MTT法檢測顯示,ASC的對數(shù)生長期為3-7d,第8d開始進(jìn)入平臺期。流式細(xì)胞術(shù)檢測結(jié)果表明,ASC細(xì)胞表達(dá)CD34(-)/CD45(-)/CD90(+)/CD105(+) /CD73(+)/CD44(+),符合間充質(zhì)干細(xì)胞表型。誘導(dǎo)分化試驗表明,ASC可以向成脂、成骨和成軟骨方向分化。CBMNCs分離后,單核細(xì)胞數(shù)量達(dá)到8.9×109,活性細(xì)胞計數(shù)結(jié)果顯示,活性細(xì)胞數(shù)占所有有核細(xì)胞的93.16%。2. 與ASC相比,HP-ASC表達(dá)多種生長因子及其受體水平增高,與干細(xì)胞特性相關(guān)的基因Klf4和Oct4略有增高,而Nanog和Sox2表達(dá)卻較后者有所降低。此外,HP-ASC中與低氧誘導(dǎo)表達(dá)相關(guān)的基因--血紅素加氧酶-1(Heme oxygenase-1,HO-1)和基質(zhì)細(xì)胞衍生因子-1(Stromal cell derived factor-1,SDF-1)均表達(dá)增高,分別為ASC組的1.38倍和1.98倍。與細(xì)胞遷移和植入相關(guān)的基因,除金屬蛋白酶組織抑制劑(Tissue inhibitor of metalloproteinase,TIMP-1)下降外,趨化因子受體-4(CXCR4),細(xì)胞間粘附分子(Intercellular cell adhesion molecule, ICAM-1和ICAM-2)的表達(dá)都有所增加。體外模擬心梗環(huán)境培養(yǎng)可以促進(jìn)HP-ASC-T表達(dá)心肌特異性標(biāo)志物(CX43, FABP4, GATA-4)和促血管生長因子(VEGF),同時也可促進(jìn)HP-ASC-T表達(dá)多種生長因子及其受體。3. 動物試驗表明,與PBS組相比,HP-ASC組和ASC組在心梗后7d及15d均可顯著減少心梗面積,增加細(xì)胞存活數(shù)量,減少凋亡細(xì)胞數(shù)量,以及顯著增加新生血管數(shù)量。而HP-ASC組較ASC組改善更為明顯。4.心梗大鼠進(jìn)行細(xì)胞移植后30天,HP-ASC組,HP-ASC+CBMNCs組和CBMNCs組均比PBS組明顯改善了心功能。其中,HP-ASC組改善效果更好。組織學(xué)檢測表明,HP-ASC組的心梗比例和心梗室壁厚度,細(xì)胞存活數(shù)量和新生血管數(shù)量均比其他對照組改善更好。[結(jié)論]1.本實驗所培養(yǎng)ASC細(xì)胞表達(dá)CD34 (-)/CD45 (-)/CD90 (+)/CD105 (+)/CD73 (+)/CD44 (+),符合間充質(zhì)干細(xì)胞表型。ASC有多向分化潛能,經(jīng)體外誘導(dǎo)可向成骨、成脂、成軟骨方向分化。離心沉降法可獲得臨床級數(shù)量的CBMNCs,分離后細(xì)胞存活率高。2.低氧預(yù)處理后,HP-ASC表達(dá)多種生長因子及其受體升高。模擬體內(nèi)心梗局部微環(huán)境可使HP-ASC表達(dá)心肌特異性標(biāo)志物、促血管生成因子和生長因子水平升高。3. 與ASC相比,HP-ASC可以更有效地減少大鼠的心梗面積,增加細(xì)胞存活比例,減少心梗區(qū)細(xì)胞凋亡數(shù)量,增加新生血管數(shù)量。4. HP-ASC對心梗大鼠心功能的改善效果比HP-ASC+CBMNCs組和CBMNCs組更好,其心梗比例和心梗室壁厚度,細(xì)胞存活數(shù)量和新生血管數(shù)量均比其他對照組改善更好。
[Abstract]:[background] myocardial infarction is a serious threat to human health. About 290 million people are suffering from cardiovascular disease every year, and 3 million 500 thousand people have died. The mortality of cardiovascular disease is the first leading cause of death in urban and rural areas in China, and is increasing year by year. At present, the main treatment means of myocardial infarction are drugs and surgery. However, they can promote vascular recanalization and reduce persistent myocardial damage, but the two have no regenerative effect on the infarcted myocardium and can not effectively reverse the fibrosis after myocardial infarction. Stem cell transplantation is a new method to promote the formation of myocardial and vascularization in the ischemic region, reduce the apoptosis of myocardial cells and reduce the ventricles. Remolding. Adipose-derived mesenchymal stem cells (ASC) has become a hot spot of current research because of its unique advantages. Although the safety and effectiveness of ASC have been preliminarily recognized, the survival and effectiveness of ASC in the body are affected by many links. Hypoxia precondition (HP) is a simple and effective way to increase the survival rate of stem cells. In order to adapt to the hypoxic environment in the infarct area, ASC in vitro can be used in vitro. Cord blood mononuclear cells (CBMNCs) can promote the angiogenesis and endothelialization of blood vessels and improve the local micro level of infarct. The revascularization of endothelial cells can bring nutrients and oxygen to the transplanted stem cells and help the stem cells to survive locally. Therefore, the combination of in vitro pretreatment and the improvement of the microenvironment in the body may be more beneficial to the long-term survival of the cells. [Objective]1. to study ASC culture, identification and differentiation ability in vitro; And CBMNCs separation and cryopreservation; 2. detection of ASC gene expression changes before and after hypoxia preconditioning; and in vitro simulated myocardial infarction environment to cultivate HP-ASC and ASC, compare the changes in the level of gene expression in the two groups; 3. evaluate whether HP-ASC is superior to ASC in the treatment of myocardial infarction in rats; 4. evaluation of HP-ASC combined CBMNCs in the treatment of myocardial infarction in rats is better than that. [method]1. with the adipose tissue after liposuction of healthy adult as the experimental object, after digestion with collagenase, the lower SVF cells were centrifuged and cultured. The cell density was measured by MTT method and the growth curve of ASC was plotted, and the flow cytometry was used to detect the surface markers of ASC cells; the osteogenesis, fat formation, and cartilage induction were respectively induced by flow cytometry. ASC differentiation was induced by the guide solution, and the multidirectional differentiation potential was detected by histochemical staining and immungo-magma staining. CBMNCs was isolated from the umbilical blood centrifugation method from healthy infants. The number of cells and the proportion of active cells were detected. The frozen reserve.2.ASC was incubated with 24h under the condition of 2%O2, and the RNA was extracted and compared with the HP-ASC and the untreated ASC gene table. To simulate the local microenvironment of myocardial infarction in the body, the heart tissue of 3D after myocardial infarction was taken after the rat myocardial infarction, pulping, adding serum and essential amino acids into the mixture of myocardial infarction. HP-ASC and ASC were cultured in the mixture of 5D to detect the change of gene expression under the induction of microenvironment; 3. 2 month old Wistar female rats, according to random The experimental animals were randomly divided into 3 groups, group HP-ASC, group ASC and group PBS, each group of 10 rats. The left anterior descending branch of the coronary artery was ligated to establish the myocardial infarction damage model. After the animal myocardial infarction was injected into the myocardium immediately after the injection of stem cells (total: 2 * 106) or PBS. cells, 5 rats were killed in each group of 7D and 15d respectively, and the heart tissue was collected and frozen to make freezing. Tissue section and paraffin tissue section were used to compare the gross morphological changes of the myocardial infarction parts, the proportion of the left ventricle in the myocardial infarction area, the cell transplantation efficiency, the number of cell apoptosis and the.4. 2 month old Wistar female rats. The experimental animals were divided into 4 groups according to the random number method, group HP-ASC, HP-ASC+CBMNCs group and CBMNCs group. And group PBS, 15 rats in each group. After the model was successfully transplanted, the total cell total was 2 x 106 (1:1). Each group was killed in 7d, 15d and 30d after operation respectively. The gross morphological changes of the myocardial infarction areas were compared, the ratio of the left ventricle and the wall thickness, and the survival rate of cell transplantation were compared. After]1. primary ASC was inoculated with 6h, some cells began to grow on the wall after 6h. After 24-48h, the cells began to appear colony like growth (CFU). After the third generation, the cells showed a typical fibroblast like appearance, and began to be whirlpool. The MTT method showed that the logarithmic growth period of ASC was 3-7d, and the 8D began to enter the platform stage. Flow formula began to flow. The results of cytometry showed that ASC cells expressed CD34 (-) /CD45 (+) /CD90 (+) /CD105 (+) /CD73 (+) /CD44 (+), which conformed to the phenotype of mesenchymal stem cells. Induced differentiation test showed that ASC could be turned into fat, bone formation and chondrogenic differentiation, and the number of mononuclear cells reached 8.9 * 109, and the number of active cells showed that the number of active cells accounted for the number of active cells. Compared with ASC, HP-ASC expressed a variety of growth factors and their receptor levels in HP-ASC, and a slight increase in Klf4 and Oct4 genes related to the characteristics of stem cells, but the expression of Nanog and Sox2 was lower than that of the latter. In addition, the genes associated with hypoxia induced expression in HP-ASC, -1 (Heme oxygenase-1, HO-1), were associated with hypoxia. The expression of -1 (Stromal cell derived factor-1, SDF-1) was increased by 1.38 and 1.98 times, respectively, in the ASC group. The expression of tercellular cell adhesion molecule, ICAM-1 and ICAM-2 increased. In vitro simulated myocardial infarction environment culture can promote the expression of HP-ASC-T specific markers (CX43, FABP4, GATA-4) and vascular growth factor (VEGF), and also promote the expression of a variety of growth factors and their receptors in HP-ASC-T. Compared with group S, 7d and 15d in group HP-ASC and ASC can significantly reduce the area of myocardial infarction, increase the number of cell survival, decrease the number of apoptotic cells, and significantly increase the number of new blood vessels. The improvement of HP-ASC group is more obvious than that of the ASC group, and 30 days after the transplantation of.4. myocardial infarction rats, HP-ASC group, HP-ASC+CBMNCs group and CBMNCs group are all more than PBS group. Significantly improved cardiac function. Among them, the HP-ASC group improved the effect better. Histological examination showed that the ratio of myocardial infarction in group HP-ASC and the thickness of myocardial infarction room wall, the number of cell survival and the number of neovascularization were better than those of the other control groups. [conclusion the ASC cells cultured in this experiment are CD34 (-) /CD45 (+) /CD105 (+) /CD73 (+) /CD44 (+) (+), +) of CD34 (-) /CD45 (+) /CD105 (+). The phenotype of mesenchymal stem cells (.ASC) has multipotential differentiation potential, which can be induced to osteogenesis, fat formation and chondrogenic differentiation in vitro. Centrifuge sedimentation can obtain a clinical level of CBMNCs. After separation, the cell survival rate is high.2. hypoxia preconditioning, HP-ASC expresses a variety of growth factors and their receptors increase. The local microenvironment of myocardial infarction can be simulated in vivo. HP-ASC expressed the specific markers of cardiac muscle, and increased the level of angiogenic factor and growth factor of.3. compared with ASC. HP-ASC could reduce the area of myocardial infarction more effectively, increase the proportion of cell survival, reduce the number of apoptosis in myocardial infarction area, and increase the effect of.4. HP-ASC on cardiac function of myocardial infarction rats than HP-ASC+CBM Group NCs and group CBMNCs were better, and their myocardial infarction ratio and myocardial infarction wall thickness, cell survival and neovascularization were all better than those of other control groups.
【學(xué)位授予單位】：中國人民解放軍醫(yī)學(xué)院
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R542.22

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