缺血
再灌注损伤
缺氧(环境)
医学
心肌梗塞
PI3K/AKT/mTOR通路
蛋白激酶B
心肌保护
LY294002型
药理学
体内
细胞凋亡
心脏病学
化学
生物
生物化学
氧气
有机化学
生物技术
作者
Lu Tang,Yingli Mo,Yunpeng Li,Yongkang Zhong,Shangfei He,Ya Zhang,Ying Tang,Shanshan Fu,Xianbao Wang,Aihua Chen
标识
DOI:10.1016/j.bbrc.2017.03.119
摘要
Ischemia/reperfusion (I/R) induces additional damage to the restoration of blood flow to ischemic myocardium. This study examined the effects of urolithin A (UA) on myocardial injury of ischemia/reperfusion in vivo and vitro and explored its underlying mechanisms. Mice were subjected to myocardial ischemia followed by reperfusion. Cells were subjected to hypoxia followed by reoxygenation. UA alleviated hypoxia/reoxygenation (H/R) injury in myocardial cells, reduced myocardial infarct size and cell death in mice after ischemia/reperfusion. Meanwhile, UA enhanced antioxidant capacity in cardiomyocytes following hypoxia/reoxygenation. UA reduced myocardial apoptosis following ischemia/reperfusion. The protection of UA was abolished by LY294002, a PI3K/Akt-inhibitor. These results demonstrated that UA alleviates myocardial ischemia/reperfusion injury probably through PI3K/Akt pathway.
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