半乳糖凝集素-3在心衰小鼠心室重构发生发展中的变化规律

目的 研究压力超负荷心衰小鼠心肌组织中半乳糖凝集素-3(Galectin-3)在心室重构中的作用.方法 选取40只成年雄性昆明小鼠,其中30只采用人工微创主动脉弓缩窄的方法建立压力超负荷心衰小鼠模型(弓缩窄组);10只行假手术作为对照组(假手术组),对两组小鼠心肌重构情况进行评价,同时应用实时荧光定量PCR法检测小鼠心肌组织Galectin-3表达的情况,并探讨Galectin-3在心衰时心室重构发生发展中的作用.结果 术后8周,与假手术组比较,弓缩窄组左心室舒张末期压(LVEDP)明显增加,差异有统计学意义(P=0.001)[1],而左心室收缩压(LVSP)和左心室压力变化最大速率(±dp/dtmax)明显下降,差异有统计学意义(P=0.001),说明模型制备成功;实时荧光定量PCR法结果显示,弓缩窄组小鼠心肌组织Galectin-3的表达较假手术组明显增强,差异有统计学意义(P=0.001).结论 Galectin-3可能在压力超负荷状态所诱发的心衰中参与心室重构,引起心肌间质胶原沉积和心肌肥厚,进而导致心力衰竭的发生和发展.

The Effect of Galectin-3 on the Ventricular Remodeling in the Mouse with Heart Failure

Objective To investigate the effect of Galectin-3 on the ventricular remodeling in the pressure-overloaded mouse with heart failure.Methods A total of 40 adult male Kun-ming mice were selected.30 of those mice were established for the pressure-overloaded mouse model with heart failure by aortic arch coarctation in a mini-invasive way and divided into the coarctation group, while the other 10 mice underwent the sham operation and divided into the control group.The myocardial remodeling of the two groups was evaluated and Real-Time Fluorescent Quantitative PCR was adopted to assay the expression of galectin-3 in myocardial tissues.Besides, the effect of galectin-3 on the development of ventricular remodeling was investigated in the pressure-overloaded mouse model with heart failure.Results On the 8th week after operation, the left ventricular end-diastolic pressure (LVEDP) increased significantly and the left ventricular systolic pressure (LVSP) and the maximum rise/fall rate of left ventricular pressure (±dp/dt max) decrease significantly in the coarctation group in comparison with the control group.The differences between the two groups were statistically significant (P=0.001), which indicated that the pressure-overloaded mouse model with heart failure was prepared successfully.The PCR results showed that the galectin-3 expression of myocardial tissues in the coarctation group was enhanced more significantly than that in the control group (P=0.001).Conclusion Galectin-3 may play a vital role in the ventricular remodeling after the pressure-overloaded heart failure by leading to collagen deposition and myocardial hypertrophy which would result in the occurrence and development of heart failure.