本文選題：心肌肥厚 + 心臟功能　； 參考：《吉林大學》2017年碩士論文

【摘要】：目的:探究羧基末端調節(jié)蛋白(CTMP)對壓力負荷誘導心肌肥厚小鼠的影響以及機制研究。方法:本實驗應用雄性、動物背景為C57BL/6的小鼠(8-10周齡,體重在23.5-27.5g)。選取α-MHC-MCM小鼠、CTMP-Flox小鼠和CTMP-CKO小鼠、CTMPTG小鼠,隨機分為兩組,一組行主動脈縮窄術(aortic biding,AB),作為AB組,另外一組作為對照組(Sham組)。4周后,檢測兩組小鼠的心功能,解剖后測量小鼠心臟質量(HW),肺部質量(LW),脛骨長度(TL)。并計算兩組小鼠心臟重量與體重的比值(HW/BW),心臟重量與脛骨長度的比值(HW/TL),以及肺臟重量與體重的比值(LW/BW)。在HE染色和PSR染色基礎上,觀察并測量心肌細胞橫截面積和心肌纖維化程度。應用Real-time PCR技術檢測反映代表心肌肥厚和心肌纖維化標志物的表達水平(ANP、BNP、β-MHC;Collagen Iα、CollagenⅢ、CTGF)。應用Western blot技術,檢測CTMP在MAPK和Akt通路的蛋白表達水平,探究CTMP影響心肌肥厚的作用機制。結果:1、在AB組,CTMP-CKO小鼠相較于對照組(α-MHC-MCM小鼠、CTMPFlox小鼠)心肌肥厚程度明顯增加,心肌細胞橫截面積和心肌膠原蛋白含量增加,心功能明顯惡化,以及心肌肥厚標志物和纖維化標志物明顯增加。2、在AB組,CTMP-TG小鼠相較于CTMP-NTG小鼠(α-MHC-MCM小鼠)心肌肥厚程度明顯減弱,心肌細胞橫截面積減小,心肌膠原蛋白含量降低,心功能好轉,以及心肌肥厚標志物和纖維化標志物明顯降低。3、在信號通路研究中,CTMP能夠影響Akt及其下游分子磷酸化水平,表明CTMP通過作用于Akt通路影響心肌肥厚。結論:CTMP能夠與Akt通路相互作用,影響AKT-GSK3β信號通路,進而影響小鼠的心肌肥厚程度、心肌細胞橫截面積、心肌纖維化程度以及心功能。
[Abstract]:Aim: to investigate the effect and mechanism of carboxyl terminal regulatory protein (CTMP) on myocardial hypertrophy induced by pressure load in mice. Methods: male C57BL / 6 mice (8-10 weeks old, weight 23.5-27.5g) were used. The 偽 -MHC-MCM mice CTMP-Flox and CTMP-CKO mice were randomly divided into two groups: one group was treated with aortic coarctation (AB) as AB group, the other group was used as control group (Sham group) after 4 weeks, the cardiac function of the two groups was measured. The heart mass (HW), lung mass (LW) and tibia length (TL) were measured after dissection. The ratio of heart weight to body weight (HW / BW), the ratio of heart weight to tibia length (HW / TL), and the ratio of lung weight to body weight (LW / BW) were calculated. On the basis of HE staining and PSR staining, the cross sectional area of myocardial cells and the degree of myocardial fibrosis were observed and measured. Real-time PCR technique was used to detect the expression level of myocardial hypertrophy and myocardial fibrosis markers (ANP-BNPs, 尾 -MHC-Collagen I 偽 Collagen 鈪，

本文編號：2086340