Abstract | INTRODUCTION:
Apelin plays an important role in the protection against myocardial ischemia-reperfusion (I/R) injury, while the mechanism still remains unclear. In the current study, we aimed to evaluate the protective effect of apelin-13, and the main mechanism. MATERIAL AND METHODS: RESULTS: For the established I/R injury model, apelin-13 and SB216763 (GSK-3β inhibitor) significantly reduced the infarct size (p < 0.05), which could be abolished by LY294002 (PI3K inhibitor), PD98059 ( MEK inhibitor) and atractyloside ( mPTP accelerator). The enhanced expression levels of p-Akt, p-ERK and p-GSK-3β caused by apelin-13 (p < 0.05) could be counteracted by LY294002 and PD98059. The reduced fluorescence intensity of TMRE in the H2O2/ apelin-13 and H2O2/ SB216763 treated groups was significantly lower (p < 0.05), indicating that apelin-13 and SB216763 could reduce the decline in mitochondrial membrane potential caused by oxidant stress, and the fluorescence intensity in the hypoxia/reoxygenation + apelin-13 group was significantly lower (p < 0.05), which suggested that apelin-13 could inhibit the mitochondrial membrane potential changes induced by hypoxia/reoxygenation. CONCLUSIONS: The protective mechanism of apelin-13 might be that inactivation of GSK-3β could inhibit the opening of mPTP by activating PI3K/Akt and ERK1/2 involved in the reperfusion injury salvage kinase (RISK) pathway.
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Authors | Shuansuo Yang, Hui Li, Lei Tang, Guanghao Ge, Jiangwei Ma, Zengyong Qiao, Huajin Liu, Weiyi Fang |
Journal | Archives of medical science : AMS
(Arch Med Sci)
Vol. 11
Issue 5
Pg. 1065-73
(Oct 12 2015)
ISSN: 1734-1922 [Print] Poland |
PMID | 26528352
(Publication Type: Journal Article)
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