Role of autophagy in myocardial reperfusion injury.
Role of autophagy in myocardial reperfusion injury.
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DOI：
10.2741/e174
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发表时间：
2010-06
期刊：
影响因子：
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通讯作者：
Yulan Jin;Hui-hua Wang;X. Cui;Yuanzhe Jin;Zhelong Xu
中科院分区：
文献类型：
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作者：
Yulan Jin;Hui-hua Wang;X. Cui;Yuanzhe Jin;Zhelong Xu
虽然自噬是由心肌缺血/再灌注诱导的，但尚不清楚自噬在缺血/再灌注期间对心肌存活是有害还是有益的。离体大鼠心脏进行30分钟的区域缺血，然后2小时的再灌注。用Western印迹法通过LC 3-II与LC 3-I的比率来确定自噬。自噬在大鼠心脏再灌注时显著，但在缺血期间不显著，表明自噬可能在再灌注阶段发挥作用。缺血或再灌注并没有增强Beclin 1的表达，这表明Beclin 1可能不是离体大鼠心脏自噬形成的关键。3-甲基腺嘌呤（3-MA），一种经典的自噬抑制剂，抑制再灌注诱导的自噬，并减少梗死面积时，在再灌注。腺苷受体激动剂NECA和吗啡在再灌注时也减少了自噬的形成以及梗死面积。这些数据表明，自噬可能在再灌注过程中发挥有害作用，调节自噬可以防止。
While autophagy is induced by myocardial ischemia/reperfusion, it is unclear whether autophagy is detrimental or beneficial to myocardial survival during ischemia/reperfusion. Isolated rat hearts were subjected to 30 min regional ischemia followed by 2 h of reperfusion. Autophagy was determined by the ratio of LC3 -II to LC3-I with Western blotting. Autophagy was prominent upon reperfusion but not during ischemia in rat hearts, indicating that autophagy may play a role during reperfusion phase. Ischemia or reperfusion did not enhance Beclin 1 expression, suggesting that Beclin 1 may not be critical for the formation of autophagy in isolated rat hearts. 3-methyladenine (3-MA), a classical inhibitor of autophagy, suppressed reperfusion-induced autophagy and reduced the infarct size when introduced at reperfusion. NECA, an agonist of adenosine receptors, and morphine also reduced the formation of autophagy as well as the infarct size when introduced at reperfusion. These data suggest that autophagy may play a detrimental role during reperfusion and that modulation of autophagy may prevent.