| Literature DB >> 28343995 |
Lu Tang1, Yingli Mo2, Yunpeng Li3, Yongkang Zhong3, Shangfei He3, Ya Zhang3, Ying Tang3, Shanshan Fu3, Xianbao Wang3, Aihua Chen4.
Abstract
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.Entities:
Keywords: Ischemia; Myocardial; PI3K/Akt; Reperfusion; Urolithin A
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Year: 2017 PMID： 28343995 DOI： 10.1016/j.bbrc.2017.03.119
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575