本文關(guān)鍵詞： 急性腦梗死 內(nèi)皮祖細(xì)胞 斑塊性質(zhì) 血管內(nèi)皮生長因子 基質(zhì)細(xì)胞衍生因子-1　出處：《安徽醫(yī)科大學(xué)》2016年碩士論文　論文類型：學(xué)位論文

【摘要】：目的動(dòng)態(tài)觀察急性腦梗死(Acute Cerebral Infarct,ACI)患者外周血內(nèi)皮祖細(xì)胞(endothelial progenitor cells, EPCs)的水平變化,同時(shí)檢測外周血血管內(nèi)皮生長因子(vascular endothelial growth factor,VEGF)和基質(zhì)細(xì)胞衍生因子-1(stromal cell-derived factor-1,SDF-1)的含量,以探討急性腦梗死后EPCs的動(dòng)員機(jī)制,為臨床缺血性腦卒中的防治提供新的思路及理論基礎(chǔ)。方法選擇2015年01月01日至2015年12月31日入住宿州市立醫(yī)院神經(jīng)內(nèi)科首次發(fā)病24h內(nèi)急性腦梗死住院患者50例,同期選擇該院體檢中心年齡配對(duì)的健康體檢者40例作為對(duì)照組。急性腦梗死患者根據(jù)TOAST分型、頸動(dòng)脈有無斑塊及斑塊性質(zhì)進(jìn)行分組,其中,TOAST分型分為3組：大動(dòng)脈粥樣硬化型(Large artery atherosclerosis,LAA)26例,心源性栓塞型(Cardioembolism,CE)5例,小動(dòng)脈閉塞型(Small artery occlusion lacunay,SAO)19例；頸動(dòng)脈有無斑塊分為2組：斑塊組38例,無斑塊組12例；斑塊組根據(jù)斑塊性質(zhì)分為2組：易損斑塊組25例和穩(wěn)定斑塊組13例。以CD133+KDR+細(xì)胞作為EPCs的標(biāo)記,進(jìn)行流式細(xì)胞分析,分別檢測急性腦梗死患者發(fā)病后第1,5,10d的外周血EPCs數(shù)量,同時(shí)采用酶聯(lián)免疫吸附法測定外周血VEGF和SDF-1的含量。EPCs變化率定義為(EPCssd-EPCs1d)與EPCs1d的比值。結(jié)果(1)腦梗死組患者外周血EPCs基線數(shù)量明顯低于對(duì)照組(t=-6.046,P0.001)；收縮壓、低密度脂蛋白可能是影響急性腦梗死組基線EPCs數(shù)量的獨(dú)立危險(xiǎn)因素。(2)腦梗死組患者TOAST各亞型外周血EPCs的基線數(shù)量均低于對(duì)照組,差異有統(tǒng)計(jì)學(xué)意義(P0.05),但TOAST各亞型之間外周血EPCs的基線數(shù)量差異無統(tǒng)計(jì)學(xué)意義(F=0.273,P=0.762)。(3)腦梗死組患者斑塊組外周血EPCs基線數(shù)量低于無斑塊組,差異有統(tǒng)計(jì)學(xué)意義(P0.05)；易損斑塊組外周血EPCs基線數(shù)量高于穩(wěn)定斑塊組,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。(4)腦梗死組患者外周血EPCs數(shù)量于第5d升高,第10d呈下降趨勢(shì)。(5)腦梗死組患者外周血VEGF、SDF-1含量于第5d升高,第10d呈降低趨勢(shì)。(6)腦梗死組患者外周血EPCs的變化率與第5d時(shí)VEGF、SDF-1含量呈正相關(guān)：第5d時(shí)VEGF含量與SDF-1含量呈正相關(guān)。結(jié)論急性腦梗死患者外周血EPCs基線數(shù)量較對(duì)照組明顯降低,EPCs可能是急性腦梗死的一項(xiàng)重要危險(xiǎn)因素。EPCs數(shù)量與頸動(dòng)脈有無斑塊、斑塊性質(zhì)具有一定相關(guān)性,表明EPCs可作為頸動(dòng)脈粥樣硬化及缺血性腦疾病的一項(xiàng)重要指標(biāo)。急性腦梗死后外周血EPCs數(shù)量增加,提示腦缺血后EPCs可從骨髓動(dòng)員至外周血中。急性腦梗死后外周血EPCs的動(dòng)員可能與VEGF、SDF-1表達(dá)增加有關(guān),三者之間可能相互作用、相互影響,共同參與缺血性腦疾病的血管新生、修復(fù)、神經(jīng)元的保護(hù)等過程,對(duì)臨床估測腦梗死患者的病情、預(yù)后具有一定的指導(dǎo)意義,可為缺血性腦卒中的治療提供一條新途徑。
[Abstract]:Objective to observe the dynamic changes of peripheral blood endothelial progenitor cells (EPCs) in patients with acute Cerebral infarction (ACI), and to detect the levels of vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1 (SDF-1) in peripheral blood of patients with acute cerebral infarction (ACI), including vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1 (-1stromal cell-derived factor-1). To explore the mobilization mechanism of EPCs after acute cerebral infarction. Methods from January 1st 2015 to December 31st 2015, 50 patients with acute cerebral infarction were admitted to the Department of Neurology, Suzhou City Hospital from January 1st 2015 to December 31st 2015. At the same time, 40 patients with age matched healthy physical examination were selected as control group. Patients with acute cerebral infarction were divided into two groups according to TOAST classification, whether carotid artery had plaques or not and the nature of plaques. Among them, TOAST was divided into 3 groups: large artery atherosclerotic LAA (n = 26), cardiac embolism (n = 5), small artery occlusion lacunayus (n = 19), carotid artery plaque (n = 38) and no plaque (n = 12). According to the plaque nature, the plaque group was divided into two groups: vulnerable plaque group (n = 25) and stable plaque group (n = 13). The number of EPCs in peripheral blood of patients with acute cerebral infarction was detected by flow cytometry with CD133 KDR cells as the marker of EPCs. At the same time, the contents of VEGF and SDF-1 in peripheral blood were determined by enzyme linked immunosorbent assay (Elisa). The change rate of EPCs was defined as the ratio of EPCssd-EPCs 1d to EPCs1d. The results showed that the number of EPCs baselines in patients with cerebral infarction was significantly lower than that in the control group (P 0.001), and the systolic blood pressure (SBP) was significantly lower than that in the control group (P < 0.05). Low density lipoprotein (LDL) may be an independent risk factor affecting baseline EPCs levels in acute cerebral infarction group. The baseline number of peripheral blood EPCs in patients with acute cerebral infarction was lower than that in control group. The difference was statistically significant (P 0.05), but there was no significant difference in the number of EPCs in peripheral blood among the subtypes of TOAST. The baseline number of EPCs in the patients with cerebral infarction was lower than that in the patients without plaque. The number of peripheral blood EPCs in the vulnerable plaque group was higher than that in the stable plaque group, and the difference was statistically significant. The level of VEGF SDF-1 in peripheral blood of patients with cerebral infarction increased on the 5th day. The change rate of EPCs in peripheral blood of patients with cerebral infarction was positively correlated with the level of VEGF SDF-1 on day 5 and the content of SDF-1 at day 5. Conclusion the baseline number of EPCs in peripheral blood of patients with acute cerebral infarction is higher than that of control group. Significant reduction of EPCs may be an important risk factor of acute cerebral infarction. The number of EPCs and carotid plaque, The character of plaques is correlated, which indicates that EPCs can be used as an important index of carotid atherosclerosis and ischemic brain disease. The number of EPCs in peripheral blood increases after acute cerebral infarction. The results suggest that EPCs can be mobilized from bone marrow to peripheral blood after cerebral ischemia. The mobilization of EPCs in peripheral blood after acute cerebral infarction may be related to the increased expression of VEGF SDF-1, which may interact with each other and participate in angiogenesis of ischemic brain disease. The process of repair and neuronal protection has a certain guiding significance for clinical evaluation of the condition and prognosis of patients with cerebral infarction and can provide a new approach for the treatment of ischemic stroke.
【學(xué)位授予單位】：安徽醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2016
【分類號(hào)】：R743.3

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