【摘要】：目的通過半乳糖凝聚素3(Gal-3)特異性競(jìng)爭(zhēng)拮抗劑——改良柑橘果膠(MCP)抑制Gal-3途徑,探討Gal-3在心功能不全心室重構(gòu)中的作用。方法將30只家兔隨機(jī)分為假手術(shù)組、心功能不全組、MCP組。結(jié)扎冠狀動(dòng)脈前降支,制作心肌梗死后心功能不全模型。模型制作成功后,MCP組用生理鹽水配置75 g/L MCP,以2 m L/(kg·d)灌胃4周;假手術(shù)組及心功能不全組給予生理鹽水2 m L/(kg·d)灌胃4周。術(shù)前及術(shù)后2、4、6周,用心臟超聲儀測(cè)定各組家兔心功能,ELISA檢測(cè)血清Gal-3、腦鈉肽(BNP)水平。實(shí)時(shí)熒光定量PCR檢測(cè)心肌組織Gal-3、膠原蛋白Ⅰ、ⅢmRNA的表達(dá),計(jì)算Ⅰ/Ⅲ比值。術(shù)后6周,Masson染色觀察心肌梗死區(qū)域組織病理學(xué)情況,Western blot檢測(cè)Gal-3、膠原蛋白Ⅰ、Ⅲ的蛋白表達(dá)。結(jié)果給藥4周后MCP組心功能較心功能不全組明顯好轉(zhuǎn)(P0.01)。心功能不全組血清Gal-3高于假手術(shù)組(P0.05),MCP組血清Gal-3較心功能不全組明顯下降(P0.05)。相關(guān)性分析顯示,心功能不全組家兔心功能左心室射血分?jǐn)?shù)與血清Gal-3呈負(fù)相關(guān)性(r=-0.841,P=0.009),左心室舒張末期內(nèi)徑與血清Gal-3呈正相關(guān)(r=0.905,P=0.002)。與心功能不全組相比,MCP組Gal-3、膠原蛋白Ⅰ、ⅢmRNA表達(dá)明顯減低(P0.05)。光學(xué)顯微鏡下心功能不全組可見心肌細(xì)胞排列紊亂,部分心肌細(xì)胞壞死、水腫,膠原大量沉積并伴有炎性細(xì)胞浸潤(rùn);MCP組可見心肌纖維增粗,排列稍整齊。心功能不全組梗死區(qū)域心肌組織Gal-3、膠原蛋白Ⅰ、Ⅲ蛋白表達(dá)明顯高于MCP組和假手術(shù)組;相關(guān)性分析顯示,心功能不全組梗死區(qū)域Gal-3與膠原蛋白Ⅲ呈正相關(guān)(r=0.793,P=0.019)。結(jié)論 Gal-3在心力衰竭心室重構(gòu)和心肌纖維化進(jìn)展中起到關(guān)鍵的作用。
[Abstract]:Objective to investigate the role of Gal-3 in ventricular remodeling by inhibiting Gal-3 pathway by modified citrus pectin (MCP), a specific competitive antagonist of galactose agglutinin 3 (Gal-3). Methods Thirty rabbits were randomly divided into sham operation group and MCP group. The anterior descending coronary artery was ligated to make the model of cardiac insufficiency after myocardial infarction. After the model was successfully made, 75 g / L MCP, was injected into the stomach with saline for 4 weeks, and the sham operation group and cardiac insufficiency group were given saline 2 mL / (kg d) for 4 weeks. The serum levels of Gal-3, brain natriuretic peptide (BNP) were measured by echocardiography and Elisa before operation and 2 weeks after operation. The expression of Gal-3, collagen 鈪，

本文編號(hào)：2200790