Li Nan, Wang Jiang, Gao Feng, Li Ai-min, Song Rong, Tian Ying, Zhu Shan-jun
Department of Cardiology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
Zhonghua Xin Xue Guan Bing Za Zhi. 2009 Dec;37(12):1108-12.
To explore the changes of expression of uncoupling protein 2 (UCP2) in pressure overload induced failure myocardium in rats.
Male SD rats were randomized into 3 groups (n = 15 each): abdominal aorta constriction (AC) 20 weeks group (H20w group), sham operation group (SH20w group) and normal control group (N group). Twenty weeks later, myocardial function was evaluated by echocardiography and hemodynamic measurements. Mitochondria in ventricular tissue were isolated by centrifugation. Adenine nucleotide pools (ATP, ADP, AMP, PCr) in myocardium were measured by high performance liquid chromatography. The expression of UCP2 in mitochondria was detected by PT-PCR and Western blot analysis.
Myocardial function was significantly decreased 20 weeks post-AC compared to SH20w group and N group. Myocardial ATP, ADP, AMP and PCr contents were also significantly decreased in H20w group than the other 2 control groups. The expression of UCP2 in myocardial mitochondria was significantly increased in H20w group and negatively correlated with ATP contents (r = -0.929, P < 0.01).
The expression of UCP2 was upregulated in pressure overload induced failure heart and might be responsible for decreased myocardial adenine nucleotide and energy metabolism disturbance in this model.
探讨解偶联蛋白2(UCP2)在压力超负荷诱导的大鼠心肌衰竭中表达的变化。
雄性SD大鼠随机分为3组(每组n = 15):腹主动脉缩窄(AC)20周组(H20w组)、假手术组(SH20w组)和正常对照组(N组)。20周后,通过超声心动图和血流动力学测量评估心肌功能。通过离心分离心室组织中的线粒体。采用高效液相色谱法测定心肌中的腺嘌呤核苷酸池(ATP、ADP、AMP、磷酸肌酸)。通过PT-PCR和蛋白质免疫印迹分析检测线粒体中UCP2的表达。
与SH20w组和N组相比,AC术后20周心肌功能显著降低。H20w组心肌ATP、ADP、AMP和磷酸肌酸含量也显著低于其他2个对照组。H20w组心肌线粒体中UCP2的表达显著增加,且与ATP含量呈负相关(r = -0.929,P < 0.01)。
在压力超负荷诱导的衰竭心脏中UCP2表达上调,可能是该模型中心肌腺嘌呤核苷酸减少和能量代谢紊乱的原因。