南方医科大学学报2016，Vol.36Issue(5)：633-638,6.
2,3-丁二酮单肟改善大鼠离体心脏钙反常损伤的作用及机制
Effect of 2,3-butanedione monoxime on calcium paradox-induced heart injury in rats
摘要
Abstract
Objective To investigate the Effect of 2,3-butanedione monoxime (BDM) on calcium paradox-induced heart injury and its underlying mechanisms. Methods Thirty-two adult male SD rats were randomized into 4 groups, namely the control group, BDM treatment control group, calcium paradox group, and BDM treatment group. Isolated Sprague Dawley male rat hearts underwent Langendorff perfusion and the left ventricular pressure (LVP) and left ventricular end-diastolic pressure (LVEDP) were monitored. Left ventricular developed pressure (LVDP) was calculated to evaluate the myocardial performance. Lactate dehydrogenase (LDH) content in the coronary flow was determined. Triphenyltetrazolium chloride staining was used to measure the infarct size, and myocardial cell apoptosis was tested with TUNEL method. Western blotting was used to determine the expression of cleaved caspase-3 and cytochrome c. Results Compared with the control group, BDM at 20 mmol/L had no effect on cardiac performance, cell death, apoptotic index or the content of LDH, cleaved caspase-3 and cytochrome c at the end of perfusion under control conditions (P>0.05). Calcium paradox treatment significantly decreased the cardiac function and the level of LVDP and induced a larger infarct size (P<0.01), an increased myocardial apoptosis index (P<0.01), and up-regulated expressions of cleaved caspase-3 and cytochrome c (P<0.01). BDM (20 mmol/L) significantly attenuated these effects induced by calcium paradox, and markedly down-regulated the levels of LVEDP and LDH (P<0.01), lowered myocardial apoptosis index, decreased the content of cleaved caspase-3 and cytochrome c (P<0.01), increased LVDP, and reduced the infarct size (P<0.01). Conclusion BDM suppresses cell apoptosis and contracture and improves heart function and cell survival in rat hearts exposed to calcium paradox, suggesting the value of BDM as an potential drug for myocardial ischemia reperfusion injury.关键词
挛缩/钙超载/2,3-丁二酮单肟/凋亡/心肌损伤Key words
calcium overload/contracture/2,3-butanedione monoxime/apoptosis/myocardial injury引用本文复制引用
孔令恒,顾晓明,苏兴利,孙娜,魏明,朱娟霞,常盼,周京军..2,3-丁二酮单肟改善大鼠离体心脏钙反常损伤的作用及机制[J].南方医科大学学报,2016,36(5):633-638,6.基金项目
国家自然科学基金（31371181）；陕西省教育厅科研计划项目（15JK1617）；西安医学院博士基金（2011DOC02）；本项目受西安医学院学科建设经费Supported by National Natural Science Foundation of China (31371181) （31371181）
