【摘要】：目的通過檢測(cè)超極化激活環(huán)核苷酸門控陽(yáng)離子通道2蛋白(HCN2)和細(xì)胞膜錨蛋白蛋白(ANK2)在心源性猝死(SCD)病人和非心源性猝死病人竇房結(jié)細(xì)胞的表達(dá)水平,初步探討HCN2蛋白和ANK2蛋白在SCD病人竇房結(jié)的表達(dá)變化及其意義。方法收集青島市市立醫(yī)院病理科2015年9月-2016年3月診斷為SCD的個(gè)體心臟27例作為研究組,其中23例為冠心病患者,4例為病毒性心肌炎患者;選擇因交通事故、外傷等所致死亡者標(biāo)本13例作為對(duì)照組。準(zhǔn)確切取心臟竇房結(jié)組織,石蠟包埋,部分HE染色,部分免疫組織化學(xué)染色,采用Mann-Whitney秩和檢驗(yàn)、t檢驗(yàn)和pearson相關(guān)系數(shù)進(jìn)行統(tǒng)計(jì)分析。結(jié)果1.竇房結(jié)病理形態(tài)學(xué)觀察:SCD組和非SCD組竇房結(jié)組織均存在不同程度的基礎(chǔ)病理改變,包括脂肪浸潤(rùn)、纖維化、動(dòng)脈狹窄、慢性炎癥、大片出血等,SCD組竇房結(jié)病理改變數(shù)量及嚴(yán)重程度遠(yuǎn)高于非SCD組,差異有統(tǒng)計(jì)學(xué)意義(p=0.0110.01)。2.竇房結(jié)HCN2蛋白的表達(dá):HCN2在竇房結(jié)組織P細(xì)胞及T細(xì)胞中均有表達(dá),HCN2在SCD組及非SCD組中均呈核旁點(diǎn)狀著色。SCD組HCN2在竇房結(jié)組織中呈棕褐色或棕黃色顆粒非均質(zhì)分布在核旁;非SCD組HCN2不表達(dá)或微量表達(dá),淡黃色細(xì)顆粒稀疏散在分布在核旁。SCD組竇房結(jié)組織HCN2蛋白表達(dá)量高于非SCD組,差異有統(tǒng)計(jì)學(xué)意義(p0.01)。3.竇房結(jié)ANK2蛋白的表達(dá):ANK2在竇房結(jié)組織定位在細(xì)胞胞漿中,在P細(xì)胞及T細(xì)胞中均有表達(dá)。SCD組ANK2微量表達(dá),稀疏分布于竇房結(jié)細(xì)胞胞漿內(nèi);非SCD組ANK2呈深黃色染色,均質(zhì)分布于細(xì)胞漿內(nèi)。SCD組ANK2蛋白表達(dá)量明顯低于對(duì)照組,差異有統(tǒng)計(jì)學(xué)意義(p0.01)。4.竇房結(jié)HCN2蛋白及ANK2蛋白表達(dá)的相關(guān)性:用pearson等級(jí)相關(guān)分析心源性猝死組HCN2、ANK2蛋白表達(dá)的相關(guān)性顯示,HCN2、ANK2蛋白的表達(dá)無(wú)明顯相關(guān)性(r=-0.453,p=0.120.05)。結(jié)論心源性猝死患者竇房結(jié)均存在不同程度的病理改變,與正常對(duì)照組相比,HCN2蛋白表達(dá)水平上調(diào),ANK2蛋白表達(dá)水平下調(diào)。我們的結(jié)果表明,離子通道蛋白表達(dá)紊亂可能導(dǎo)致嚴(yán)重心律失常從而成為發(fā)生心源性猝死的重要原因。意義本文章以人體心臟標(biāo)本做研究,探討了HCN2及ANK2通道蛋白在心源性猝死者竇房結(jié)組織中的表達(dá)水平,克服了以往的以動(dòng)物模型為研究的局限性。實(shí)驗(yàn)結(jié)果表明,HCN2及ANK2在蛋白質(zhì)水平的表達(dá)異�？赡芘cSCD的發(fā)生相關(guān),為不明原因性SCD的診斷提供了重要的參考價(jià)值,為病人尋找死因提供幫助,而且對(duì)早期預(yù)防及治療心源性猝死有一定的幫助。
[Abstract]:Objective to detect the expression of hyperpolarization activated cyclic nucleotides gated cationic channel 2 protein (HCN2) and cell membrane anchor protein (ANK2) in sinoatrial node cells of patients with sudden cardiac death (SCD) and patients with non-cardiac sudden death. To investigate the expression and significance of HCN2 protein and ANK2 protein in sinoatrial node of SCD patients. Methods from September 2015 to March 2016, 27 individual hearts diagnosed as SCD were collected as the study group, including 23 patients with coronary heart disease and 4 patients with viral myocarditis. Thirteen cases of death caused by traffic accidents and trauma were selected as control group. Cardiac sinoatrial node tissue was accurately resected, paraffin embedded, partial HE staining and partial immunohistochemical staining. Mann-Whitney rank sum test, t test and pearson correlation coefficient were used for statistical analysis. Result 1. Pathomorphological observation of sinoatrial node: there were basic pathological changes in sinoatrial node tissue in SCD group and non-SCD group, including fat infiltration, fibrosis, arterial stenosis, chronic inflammation, massive hemorrhage and so on. The number and severity of pathological changes of sinoatrial node in SCD group were much higher than those in non-SCD group (p 鈮，

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