Journal
ACTA PHARMACOLOGICA SINICA
Volume 35, Issue 12, Pages 1504-1513Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/aps.2014.78
Keywords
heart; myocardium; ischemia-reperfusion injury; inhalational anesthetic; sevoflurane; post-conditioning; ERK1/2; PD98059; oncosis; apoptosis
Funding
- National Natural Science Foundation of China [81372024]
- Technology Bureau of Suzhou, China [SYS201130, SYSD2012085, KJXW2011015, SYS201125, SYS201340]
- Revitalizing the Key Talent's Subsidy Project in Science and Education (Jiangsu Province, China)
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Aim: To investigate the role of extracellular signal-regulated kinases (ERKs) in sevoflurane post-conditioning induced cardioprotection in vitro. Methods: Isolated rat hearts were subjected to 30 min ischemia followed by 120 min reperfusion (I/R). Sevoflurane post-conditioning was carried out by administration of O-2-enriched gas mixture with 3% sevoflurane (SEVO) for 15 min from the onset of reperfusion. Cardiac functions, myocardial infarct size, myocardial ATP and NAD(+) contents, mitochondrial ultrastructure, and anti-apototic and anti-oncosis protein levels were measured. Results: Sevoflurane post-conditioning significantly improved the heart function, decreased infarct size and mitochondria damage, and increased myocardial ATP and NAD(+) content in the I/R hearts. Furthermore, sevoflurane post-conditioning significantly increased the levels of p-ERK and p-p70S6K, decreased the levels of porimin, caspase-8, cleaved caspase-3, and cytosolic cytochrome c in the I/R hearts. Co-administration of the ERK1/2 inhibitor PD98059 (20 mu mol/L) abolished the sevoflurane-induced protective effects against myocardial I/R. Conclusion: Sevoflurane post-conditioning protects isolated rat hearts against myocardial I/R injury and inhibits cell oncosis and apoptosis via activation of the ERK1/2 pathway.
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