Apelin-13对急性缺血诱导的大鼠心肌细胞凋亡的影响
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The Effect of Apelin-13 on Ischemia-Induced Cardiomyocyte Apoptosis in Acute Myocardial Ischemia Rats
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    目的研究Apelin在大鼠急性心肌缺血时的变化及外源性给予Apelin-13对大鼠急性心肌缺血损伤的保护机制。方法采用酶联免疫吸附法测定大鼠前降支结扎30、60和120min时心肌组织及血浆Apelin含量;并通过结扎大鼠前降支120min建立急性心肌缺血模型,于缺血前5min经尾静脉分别注射10、100μg/kgApelin-13,观察Apelin-13对心脏功能、心肌细胞凋亡及Bcl-2、Bax和Caspase-3表达的影响。结果心肌缺血30~60min时,大鼠心肌组织Apelin含量逐渐增高,而缺血120min时Apelin含量降至正常水平以下,血浆中Apelin含量在缺血120min内呈逐渐增高趋势。缺血前给予100μg/kgApelin-13能改善心脏功能,减少心肌细胞凋亡,抑制促凋亡基因Bax和Caspase-3的表达,并提高抗凋亡基因Bcl-2的表达。结论在心肌缺血早期心肌组织Apelin含量代偿性增高,长时间缺血时含量下降;外源性Apelin-13在急性心肌缺血中的保护作用与抑制心肌细胞凋亡有关。

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    Aim To determine the content of apelin in acute myocardial ischemia and probe the protective mechanism of exogenous apelin-13 on myocardium ischemic injury in rats. Methods The content of apelin in myocardium and plasma was detected by enzyme linked immunosorbent assay (ELISA) in SD rats suffered from myocardial ischemia by ligating the left anterior descending coronary artery (LAD) for 30, 60 and 120 min respectively. Then the rats were randomly divided into sham operated group, model control group and two apelin-13 groups, to which apelin-13 of 10 and 100 μg/kg was infused via caudal vein 5 min before a 120 min-myocardial ischemia. The cardial function was measured by electrophysiolograph. Cardiomyocyte apoptosis was detected with TUNEL and Bcl-2, Bax and Caspase-3 protein expression of myocardium with Western blotting. Results The content of apelin in myocardium was markedly increased during myocardial ischemia 30 to 60 min and decreased to below basal level on ischemia 120 min (P<0.01). The content of apelin in plasma increased gradually during myocardial ischemia 30 to 120 min (P<0.01). In myocardial ischemia models induced by ligating LAD for 120 min, apelin-13 (100 μg/kg) infused pre-ischemia can significantly improve cardial function, inhibit the cardiomyocyte apoptosis (P<0.01), increase Bcl-2 protein expression and decrease Bax and Caspase-3 protein expression. Conclusion The content of apelin in myocardium was increased in a compensatory role in early myocardial ischemia and decreased in sustained myocardial ischemia. The protective mechanism of exogenous apelin-13 on ischemic myocardium may be related to inhibition of cardiomyocyte apoptosis.

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张志,于波. Apelin-13对急性缺血诱导的大鼠心肌细胞凋亡的影响[J].中国动脉硬化杂志,2008,16(9):693~696.

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  • 收稿日期:2008-07-21
  • 最后修改日期:2008-09-12
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