Abstract:
:Anesthetic cardioprotection reduces myocardial infarct size following ischemia-reperfusion injury. However, the underlying mechanisms that drive ischemia-reperfusion injury in cardiomyocytes remain unclear. In this study, we report that isoflurane, a commonly used inhaled anesthetic, can protect cardiomyocytes from anoxia/reoxygenation injury by a nucleotide binding oligomerization domain containing 2 (NOD2)-dependent mechanism. The results showed that isoflurane increased cell viability, and decreased autophagosome generation in primary cardiomyocytes under anoxia/reoxygenation conditions. In addition, western blot revealed that isoflurane reduces the expression of NOD2. Overexpression of NOD2 is accompanied by an increased expression of autophagy-related genes, decreased cell viability, and enhanced expression of phosphorylation p38-mitogen-activated protein kinase (p38MAPK), while NOD2 knockdown exerted the opposite effect. Following preconditioning with SB203580, a p38MAPK inhibitor, the inhibitory effect of isoflurane on cardiomyocytes autophagy was further enhanced, which suggests that p38MAPK is involved in the mechanism of cardioprotection provided by isoflurane. These findings reveal a novel mechanism underlying isoflurane-afford protection of myocardial injury.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Yang C,Jiao Y,Yan N,Wu B,Ren Y,Li H,Sun J,Gao Jdoi
10.1016/j.neulet.2016.11.031subject
Has Abstractpub_date
2017-01-10 00:00:00pages
154-160eissn
0304-3940issn
1872-7972pii
S0304-3940(16)30883-7journal_volume
637pub_type
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