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急性腦梗死患者外周血內皮祖細胞的水平變化及相關性研究

發(fā)布時間:2018-02-12 04:14

  本文關鍵詞: 急性腦梗死 內皮祖細胞 斑塊性質 血管內皮生長因子 基質細胞衍生因子-1 出處:《安徽醫(yī)科大學》2016年碩士論文 論文類型:學位論文


【摘要】:目的動態(tài)觀察急性腦梗死(Acute Cerebral Infarct,ACI)患者外周血內皮祖細胞(endothelial progenitor cells, EPCs)的水平變化,同時檢測外周血血管內皮生長因子(vascular endothelial growth factor,VEGF)和基質細胞衍生因子-1(stromal cell-derived factor-1,SDF-1)的含量,以探討急性腦梗死后EPCs的動員機制,為臨床缺血性腦卒中的防治提供新的思路及理論基礎。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)院神經內科首次發(fā)病24h內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的健康體檢者40例作為對照組。急性腦梗死患者根據TOAST分型、頸動脈有無斑塊及斑塊性質進行分組,其中,TOAST分型分為3組:大動脈粥樣硬化型(Large artery atherosclerosis,LAA)26例,心源性栓塞型(Cardioembolism,CE)5例,小動脈閉塞型(Small artery occlusion lacunay,SAO)19例;頸動脈有無斑塊分為2組:斑塊組38例,無斑塊組12例;斑塊組根據斑塊性質分為2組:易損斑塊組25例和穩(wěn)定斑塊組13例。以CD133+KDR+細胞作為EPCs的標記,進行流式細胞分析,分別檢測急性腦梗死患者發(fā)病后第1,5,10d的外周血EPCs數量,同時采用酶聯(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。結果(1)腦梗死組患者外周血EPCs基線數量明顯低于對照組(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數量的獨立危險因素。(2)腦梗死組患者TOAST各亞型外周血EPCs的基線數量均低于對照組,差異有統(tǒng)計學意義(P0.05),但TOAST各亞型之間外周血EPCs的基線數量差異無統(tǒng)計學意義(F=0.273,P=0.762)。(3)腦梗死組患者斑塊組外周血EPCs基線數量低于無斑塊組,差異有統(tǒng)計學意義(P0.05);易損斑塊組外周血EPCs基線數量高于穩(wěn)定斑塊組,差異有統(tǒng)計學意義(P0.05)。(4)腦梗死組患者外周血EPCs數量于第5d升高,第10d呈下降趨勢。(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。(6)腦梗死組患者外周血EPCs的變化率與第5d時VEGF、SDF-1含量呈正相關:第5d時VEGF含量與SDF-1含量呈正相關。結論急性腦梗死患者外周血EPCs基線數量較對照組明顯降低,EPCs可能是急性腦梗死的一項重要危險因素。EPCs數量與頸動脈有無斑塊、斑塊性質具有一定相關性,表明EPCs可作為頸動脈粥樣硬化及缺血性腦疾病的一項重要指標。急性腦梗死后外周血EPCs數量增加,提示腦缺血后EPCs可從骨髓動員至外周血中。急性腦梗死后外周血EPCs的動員可能與VEGF、SDF-1表達增加有關,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、神經元的保護等過程,對臨床估測腦梗死患者的病情、預后具有一定的指導意義,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.
【學位授予單位】:安徽醫(yī)科大學
【學位級別】:碩士
【學位授予年份】:2016
【分類號】:R743.3

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