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Biochem Biophys Res Commun. 2017 May 6;486(3):774-780. doi: 10.1016/j.bbrc.2017.03.119. Epub 2017 Mar 23.

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

Author information

1
Department 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.
2
Department of Internal Medicine, Yiyang Medical College, Yingbin Road 516, Yiyang, Hunan 413000, China; Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
3
Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Gongye Road, Guangzhou 510280, China.
4
Department of Cardiology, Zhujiang Hospital of Southern Medical University, No. 253, Gongye Road, Guangzhou 510280, China. Electronic address: aihuachenzjphd@hotmail.com.

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.

KEYWORDS:

Ischemia; Myocardial; PI3K/Akt; Reperfusion; Urolithin A

PMID:
28343995
DOI:
10.1016/j.bbrc.2017.03.119
[Indexed for MEDLINE]

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