解耦联蛋白-2与压力超负荷大鼠心肌肥厚中的细胞凋亡

Uncoupling protein-2 and apoptosis in pressure overload-induced cardiac hypertrophy in rats

目的探讨心肌解耦联蛋白-2(UCP2)与压力超负荷心肌肥厚中心肌细胞凋亡的关系。方法采用腹主动脉缩窄法建立大鼠压力超负荷模型,假手术大鼠作为对照组。术后1,2,4,7,14,21,30d,RT-PCR法测定UCP2mRNA含量,TUNEL法检测心肌细胞凋亡水平。结果(1)与对照组比较,压力超负荷组在术后4d UCP2 mRNA含量上调,并持续增高至30d。(2)压力超负荷组心肌细胞凋亡在术后1d即升高,在4d时进入高峰期并持续至7d,其后低水平持续存在,直至实验结束。而对照组未发现凋亡细胞。结论UCP2可能参与了压力超负荷心肌肥厚中细胞凋亡的调控,但其确切机制有待进一步研究。

Objective To explore the relationship between uncoupling protein-2 （UCP2） and apoptosis in pressure overload-induced cardiac hypertrophy. Methods The pressure overload animal model was established in rats by abdomial aorta coarctation and an equal number of sham-operated rats served as controls. The time course was 1, 2, 4, 7, 14, 21 and 30 days after operation. The UCP2 mRNA expression was evaluated by RT-PCR. The TUNEL method was applied to detect the myocardial apoptosis. Results （1） Compared with control group, the expression of UCP2 mRNA was upregulated at 4 days, and developed progressively to 30 days. （2） The apoptosis increased significantly at d 1, and reached a plateau between d 4-d 7 ; afterwards, it decreased continuously to low level. However, the apoptosis was so rare that it was undetectable in control group. Conclusion Although the precise role for UCP2 need to be clarified in the future works, it may participate in the regulation of apoptosis during the pressure overload-induced cardiac hvpertrophy.