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Biochemical and Biophysical Research Communications 2017-May

Urolithin A alleviates myocardial ischemia/reperfusion injury via PI3K/Akt pathway.

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Krækjan er vistuð á klemmuspjaldið
Lu Tang
Yingli Mo
Yunpeng Li
Yongkang Zhong
Shangfei He
Ya Zhang
Ying Tang
Shanshan Fu
Xianbao Wang
Aihua Chen

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Útdráttur

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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