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Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Urolithin A alleviates myocardial ischemia/reperfusion injury via PI3K/Akt pathway
Lu Tang1, Yingli Mo2, Yunpeng Li3
1Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Gongye Road, Guangzhou 510280, China; Department of Cardiology, Yiyang Central Hospital, Kangfu Road 118, Yiyang, Hunan 413000, China.
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.
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