Das D K, Barua P K, Jones R M
Department of Surgery, University of Connecticut School of Medicine, Farmington 06032.
Biochim Biophys Acta. 1991 Mar 4;1073(2):394-401. doi: 10.1016/0304-4165(91)90148-a.
In an attempt to resolve the issue of whether there is a loss of fatty acid binding protein (H-FABP) from heart during ischemia and reperfusion, and to further examine the role of this protein in ischemic-reperfusion injury, the amount of H-FABP of heart was monitored during ischemia and reperfusion. Excellent correlation was obtained between the loss of H-FABP from heart and its appearance in the perfusate buffer when examined by Western blot using the specific antibody to H-FABP. Further quantitation was achieved by densitometric scanning of the Western blot and rocket electrophoresis. Maximum release of H-FABP was observed within 20 min of reperfusion, the total release being 10% of the H-FABP content of the heart. Mepacrine, a membrane stabilizer and a phospholipase inhibitor, reduced the release of H-FABP from the heart and prevented the accumulation of nonesterified fatty acids in the tissue during ischemia and reperfusion. In view of the established role of H-FABP in the preservation of membrane phospholipids by either scavenging free radicals during ischemia and reperfusion or by modulating the enzymes of phospholipid synthesis, it seems likely that the loss of H-FABP may have some contribution towards the ischemic-reperfusion injury.
为了确定在缺血和再灌注过程中心脏是否存在脂肪酸结合蛋白（H-FABP）丢失的问题，并进一步研究该蛋白在缺血再灌注损伤中的作用，对缺血和再灌注过程中心脏H-FABP的含量进行了监测。当使用针对H-FABP的特异性抗体通过蛋白质印迹法检测时，心脏中H-FABP的丢失与其在灌注缓冲液中的出现之间具有良好的相关性。通过对蛋白质印迹和火箭电泳进行光密度扫描实现了进一步的定量分析。在再灌注20分钟内观察到H-FABP的最大释放，总释放量为心脏H-FABP含量的10%。膜稳定剂和磷脂酶抑制剂米帕林减少了心脏中H-FABP的释放，并防止了缺血和再灌注期间组织中非酯化脂肪酸的积累。鉴于H-FABP在缺血和再灌注期间通过清除自由基或调节磷脂合成酶来保护膜磷脂方面已确定的作用，H-FABP的丢失似乎可能对缺血再灌注损伤有一定影响。
