Myocardial Iron Metabolism in the Regulation of Cardiovascular Diseases in Rats
Myocardial Iron Metabolism in the Regulation of Cardiovascular Diseases in Rats
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DOI：
10.1159/000315077
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发表时间：
2006-01
影响因子：
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通讯作者：
N. Zhao;Zhi-dan Sun;Yuyi Mao;P. Hang;Xinlu Jiang;Lihua Sun;Jinlong Zhao;Zhimin Du
中科院分区：
文献类型：
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作者：
N. Zhao;Zhi-dan Sun;Yuyi Mao;P. Hang;Xinlu Jiang;Lihua Sun;Jinlong Zhao;Zhimin Du
铁稳态在心脏功能中起重要作用。为了了解它在糖尿病和缺血性心肌损伤中的作用，我们研究了糖尿病和心肌缺血大鼠心肌铁代谢。采用高脂饲料灌胃后腹腔注射链脲佐菌素（STZ）诱导糖尿病大鼠模型，同时结扎缺血大鼠心脏，分别结扎冠状动脉0.5、1、6、12和24 h。火焰原子吸收光谱法测定STZ诱导的糖尿病大鼠血清和心肌铁含量明显升高，肝脏铁含量明显降低。糖尿病大鼠血清超氧化物歧化酶（SOD）、丙二醛（MDA）和铁蛋白水平升高。二价金属转运蛋白1（DMT 1）的蛋白水平降低，而转铁蛋白受体（TfR）和金属转运蛋白1（MTP 1）的蛋白水平升高。相反，在缺血大鼠中未观察到铁浓度的改变。DMT1、TfR和MTP1在心肌梗死后表达无明显变化。结果提示，糖尿病（DM）可引起心肌铁超载，至少部分是通过上调TfR引起的。同时，通过下调DMT 1和上调MTP 1的表达来减轻心肌中过量的铁。然而，心肌梗死（MI）并没有打破心肌铁的平衡。总之，铁稳态在DM和MI中的反应不同。
The iron homeostasis plays an important role in cardiac function. To understand how it acts in diabetic and ischemic myocardial injury, we studied the myocardial iron metabolism in diabetic and myocardial ischemic rats. Diabetic rats were induced by intraperitoneal injection of streptozocin (STZ) after intragastric administration of a high-fat diet while the ischemic rat hearts were subjected to coronary artery ligation for 0.5, 1, 6, 12 or 24 h, respectively. In STZ-induced diabetic rats, the contents of serum and myocardial iron were found elevated obviously accompany with the decrease of hepatic iron determined by the flame emission atomic absorption spectroscopy. The levels of superoxide dismutase (SOD), malonaldehyde (MDA) and serum ferritin were increased in diabetic rats. Moreover, protein level of divalent metal transporter 1 (DMT1) was decreased while that for transferrin receptor (TfR) and metal transporter protein 1 (MTP1) was increased. In contrast, no alteration of iron concentration was observed in the ischemic rats. The expression of DMT1, TfR and MTP1 has not changed after infraction. The findings suggested that diabetes mellitus (DM) induced the iron overload in the myocardium, at least in part by up-regulation of TfR. Meanwhile, down-regulation of DMT1 and up-regulation of MTP1 were induced to alleviate the excessive iron in the myocardium. However, myocardial infraction (MI) has not broken the balance of myocardial iron. In conclusion, the iron homeostasis reacts differently in DM and MI.