S100A4蛋白和P53蛋白在肥厚型心肌病導(dǎo)致的心肌纖維化中的表達(dá)及意義
發(fā)布時(shí)間:2018-03-09 22:43
本文選題:S100A4 切入點(diǎn):P53 出處:《青島大學(xué)》2016年碩士論文 論文類型:學(xué)位論文
【摘要】:【目的】心肌纖維化是肥厚型心肌病的典型病理改變之一,而S100A4、P53蛋白與心肌纖維化的發(fā)生聯(lián)系密切。本實(shí)驗(yàn)旨在研究肥厚型心肌病患者者心肌細(xì)胞中S100A4、P53蛋白的表達(dá),探討其與肥厚型心肌病心肌纖維化的關(guān)系!痉椒ā窟x擇于2013年1月-2014年6月就診于北京阜外心血管醫(yī)院的肥厚性心肌病手術(shù)患者10例作為HCM組,另選擇10例于青島地區(qū)交通事故及高墜致死者心肌組織為健康對(duì)照組,運(yùn)用苦味酸天狼猩紅染色法比較兩組的膠原容積分?jǐn)?shù)、原位雜交方法檢測S100A4和P53 m RNA表達(dá)情況以及運(yùn)用免疫組化法比較2組心肌組織內(nèi)S100A4、P53陽性表達(dá)的變化;運(yùn)用原位雜交方法檢測S100A4、P53 m RNA表達(dá)情況。利用Image-Pro Plus 6.0等圖像分析軟件進(jìn)行染色結(jié)果分析。統(tǒng)計(jì)結(jié)果進(jìn)行t檢驗(yàn),以P0.01表示為存在顯著性差異!窘Y(jié)果】HCM組心肌間質(zhì)膠原容積分?jǐn)?shù)高于對(duì)照組(t=4.105,P0.01),HCM組心肌細(xì)胞S100A4、P53蛋白表達(dá)明顯高于對(duì)照組(t=7.628,P0.01)以及二者m RNA陽性表達(dá)均高于對(duì)照組(t=3.464,P0.01)差異均有高度統(tǒng)計(jì)學(xué)意義!窘Y(jié)論】S100A4、P53蛋白的過度表達(dá)可能在HCM心肌纖維化過程中發(fā)揮重要作用,可能為肥厚型心肌病心肌纖維化的治療提供新的方向。
[Abstract]:[objective] Myocardial fibrosis is one of the typical pathological changes in hypertrophic cardiomyopathy. To investigate the relationship between hypertrophic cardiomyopathy and myocardial fibrosis. [methods] Ten patients with hypertrophic cardiomyopathy treated in Fuwei Cardiovascular Hospital from January 2013 to June 2014 were selected as HCM group. In addition, 10 cases of myocardial tissue in Qingdao area were selected as the healthy control group. The collagen volume fraction of the two groups was compared by picric acid sirius red staining method. In situ hybridization was used to detect the expression of S100A4 and p53 m RNA, and immunohistochemical method was used to compare the expression of S100A4 and p53 in myocardium. In situ hybridization method was used to detect the expression of p53 m RNA in S100A4, and the staining results were analyzed by Image-Pro Plus 6.0 and other image analysis softwares. The statistical results were analyzed by t test. [results] the myocardial interstitial collagen volume fraction in the HCM group was significantly higher than that in the control group (t 4.105 and P 0.01), and the expression of S100A4P 53 protein in the HCM group was significantly higher than that in the control group (P 0.01), and the positive expression of m RNA was higher than that in the control group (t 3.464P 0.01). [conclusion] the overexpression of S100A4 protein may play an important role in the process of myocardial fibrosis in HCM. It may provide a new direction for the treatment of hypertrophic cardiomyopathy.
【學(xué)位授予單位】:青島大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2016
【分類號(hào)】:D919
【參考文獻(xiàn)】
相關(guān)期刊論文 前2條
1 馮相平;董文彬;陳新山;;冠心病猝死冠狀動(dòng)脈粥樣硬化斑塊單核細(xì)胞趨化蛋白1表達(dá)的研究[J];中華心血管病雜志;2006年07期
2 孟曉慧,汪翼,于永慧,陳瑤,馬沛然;病毒性心肌炎小鼠血管緊張素的改變與心肌膠原的關(guān)系[J];醫(yī)學(xué)臨床研究;2004年04期
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