To investigate the role of melatonin in calcium overload-induced heart injury. Methods: Thirty-two rats were divided into 4 groups: a control group (Control), a melatonin control group (Mel), a calcium overload group (CaP), and a calcium overload plus melatonin group (Mel+CaP). Isolated Sprague Dawley male rat hearts underwent Langendorff perfusion. Left ventricular developed pressure (LVDP) was calculated to evaluate the myocardial performance. Triphenyltetrazolium chloride staining was used to measure the infarct size of myocardium. Lactate dehydrogenase (LDH) activity in the coronary flow was determined. The expressions of caspase-3 and cytochrome c were determined by Western blot. The pathological morphological changes in myocardial fiber were analyzed by HE staining. Results: Compared with the control group, calcium overload significantly induced an enlarged infarct size (P<0.01), accompanied by the disordered arrangement of myocardial fiber, up-regulation of cytochrome c and caspase-3 (P<0.01), and the increased activity of LDH (P<0.01). These effects were significantly attenuated by 10 μmol/L melatonin (P<0.01). Conclusion: Melatonin can alleviate calcium overload-induced heart injury.
目的：观察褪黑素(melatonin，Mel)对大鼠离体心脏急性钙超载损伤的保护作用。方法：将32只大鼠随机分为4组：对照组(Control)、褪黑素组(Mel)、钙反常组(calcium paradox，CaP)和Mel干预钙反常组(Mel+CaP)。大鼠离体心脏行Langendorff灌流，建立钙反常模型；观察左室发展压、心肌梗死面积、乳酸脱氢酶(lactate dehydrogenase，LDH)活性、细胞色素c及caspase-3蛋白的表达变化；HE染色观察心肌纤维形态学变化。结果：与Control组相比，CaP组心肌几乎全部梗死(P<0.01)，冠状动脉流出液中LDH活性显著增加(P<0.01)，心肌纤维排列紊乱，细胞色素c和caspase-3蛋白表达均上调(P<0.01)；Mel(10 μmol/L)干预钙反常组心脏损伤各项指标均明显降低(P<0.01)。结论：Mel可明显减轻大鼠离体心脏急性钙超载诱导的损伤。.