Du Ying, Ko Kam Ming
Department of Biochemistry, Hong Kong University of Science & Technology, Clear Water Bay, Hong Kong, China.
Mol Cell Biochem. 2006 Aug;288(1-2):135-42. doi: 10.1007/s11010-006-9129-3. Epub 2006 Apr 1.
Using an ex vivo rat heart model of ischemia-reperfusion (I-R) injury, we examined the effect of pharmacological preconditioning by chronic treatment with emodin (EMD)/oleanolic acid (OA) at low dose (25 micromol/kg/day x 15) and/or ischemic preconditioning (IPC) (4 cycles of 5 min ischemia followed by 5 min of reperfusion) on myocardial I-R injury. The results indicated that EMD/OA pretreatment, IPC, or their combinations (EMD+IPC and OA+IPC) protected against myocardial I-R injury, as assessed by lactate dehydrogenase leakage and contractile force recovery. The cardioprotection was associated with a differential enhancement in mitochondrial antioxidant components. The combined EMD/OA and IPC pretreatment produced cardioprotective action in a semi-additive manner. This suggested that EMD/OA pretreatment and IPC protected against myocardial I-R injury via a similar but not identical biochemical mechanism.
利用离体大鼠心脏缺血再灌注(I-R)损伤模型,我们研究了低剂量(25微摩尔/千克/天×15)大黄素(EMD)/齐墩果酸(OA)长期治疗的药理学预处理和/或缺血预处理(IPC)(5分钟缺血后再灌注5分钟,共4个周期)对心肌I-R损伤的影响。结果表明,通过乳酸脱氢酶泄漏和收缩力恢复评估,EMD/OA预处理、IPC或它们的组合(EMD+IPC和OA+IPC)可保护心肌免受I-R损伤。心脏保护作用与线粒体抗氧化成分的差异性增强有关。EMD/OA与IPC联合预处理以半相加方式产生心脏保护作用。这表明EMD/OA预处理和IPC通过相似但不完全相同的生化机制保护心肌免受I-R损伤。