Pharmacological postconditioning with tanshinone IIA attenuates myocardial ischemia‑reperfusion injury in rats by activating the phosphatidylinositol 3‑kinase pathway

Yuan,Xun; Jing,Songbo; Wu,Lingzhen; Chen,Lianglong; Fang,Jun

doi:10.3892/etm.2014.1820

Pharmacological postconditioning with tanshinone IIA attenuates myocardial ischemia‑reperfusion injury in rats by activating the phosphatidylinositol 3‑kinase pathway

Authors:
- Xun Yuan
- Songbo Jing
- Lingzhen Wu
- Lianglong Chen
- Jun Fang
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Affiliations: Department of Cardiology, Fujian Medical University Union Hospital, Fujian Institute of Coronary Heart Disease, Fuzhou, Fujian 350001, P.R. China
Published online on: July 2, 2014 https://doi.org/10.3892/etm.2014.1820
Pages: 973-977

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Abstract

Tanshinone IIA, one of the active ingredients in the Chinese medicine Danshen, is cardioprotective when applied prior to sustained myocardial ischemia. The present study aimed to investigate whether pharmacological postconditioning with tanshinone IIA attenuates myocardial ischemia‑reperfusion injury when applied prior to prolonged reperfusion following a sustained ischemia. A total of 88 Sprague‑Dawley rats received 30 min myocardial ischemia followed by 5 or 120 min reperfusion. Compared with the ischemia‑reperfusion model group, the group that received an intravenous injection of 10 mg/kg tanshinone IIA prior to reperfusion had a reduced myocardial infarct size, higher levels of phospho‑Akt and phospho‑endothelial nitric oxide synthase and less reduction in the optical density of the mitochondria at 540 nm, indicating that the mitochondrial permeability transition (MPT) was attenuated. The cardioprotective effect conferred by tanshinone IIA was abolished by LY294002, a specific inhibitor of phosphatidylinositol 3‑kinase (PI3K). These results demonstrate that tanshinone IIA postconditioning protects the myocardium from ischemia‑reperfusion injury through the PI3K/Akt pathway, and the MPT may be also involved in this process.

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