TY - JOUR
T1 - Stearic acid methyl ester affords neuroprotection and improves functional outcomes after cardiac arrest
AU - Chen, Po Yi
AU - Wu, Celeste Yin Chieh
AU - Clemons, Garrett A.
AU - Citadin, Cristiane T.
AU - Couto e Silva, Alexandre
AU - Possoit, Harlee E.
AU - Azizbayeva, Rinata
AU - Forren, Nathan E.
AU - Liu, Chin Hung
AU - Rao, K. N.Shashanka
AU - Krzywanski, David M.
AU - Lee, Reggie Hui Chao
AU - Neumann, Jake T.
AU - Lin, Hung Wen
N1 - Funding Information:
This work was supported by grants from the American Heart Association (AHA, 19TPA34850047 , 17GRNT33660336 , 19CDA3466032 , 19POST34380784 , 19PRE34380808 ), and Louisiana State University Research Council and Joanna G. Magale Foundation .
Publisher Copyright:
© 2020 Elsevier Ltd
PY - 2020/8
Y1 - 2020/8
N2 - Cardiac arrest causes neuronal damage and functional impairments that can result in learning/memory dysfunction after ischemia. We previously identified a saturated fatty acid (stearic acid methyl ester, SAME) that was released from the superior cervical ganglion (sympathetic ganglion). The function of stearic acid methyl ester is currently unknown. Here, we show that SAME can inhibit the detrimental effects of global cerebral ischemia (i.e. cardiac arrest). Treatment with SAME in the presence of asphyxial cardiac arrest (ACA) revived learning and working memory deficits. Similarly, SAME-treated hippocampal slices after oxygen-glucose deprivation inhibited neuronal cell death. Moreover, SAME afforded neuroprotection against ACA in the CA1 region of the hippocampus, reduced ionized calcium-binding adapter molecule 1 expression and inflammatory cytokines/chemokines, with restoration in mitochondria respiration. Altogether, we describe a unique and uncharted role of saturated fatty acids in the brain that may have important implications against cerebral ischemia.
AB - Cardiac arrest causes neuronal damage and functional impairments that can result in learning/memory dysfunction after ischemia. We previously identified a saturated fatty acid (stearic acid methyl ester, SAME) that was released from the superior cervical ganglion (sympathetic ganglion). The function of stearic acid methyl ester is currently unknown. Here, we show that SAME can inhibit the detrimental effects of global cerebral ischemia (i.e. cardiac arrest). Treatment with SAME in the presence of asphyxial cardiac arrest (ACA) revived learning and working memory deficits. Similarly, SAME-treated hippocampal slices after oxygen-glucose deprivation inhibited neuronal cell death. Moreover, SAME afforded neuroprotection against ACA in the CA1 region of the hippocampus, reduced ionized calcium-binding adapter molecule 1 expression and inflammatory cytokines/chemokines, with restoration in mitochondria respiration. Altogether, we describe a unique and uncharted role of saturated fatty acids in the brain that may have important implications against cerebral ischemia.
KW - Asphyxial cardiac arrest (ACA)
KW - Cerebral ischemia
KW - Hippocampus
KW - Long chain saturated fatty acid
KW - Neuroinflammation
KW - Neuroprotection
KW - Stearic acid methyl ester (SAME)
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U2 - 10.1016/j.plefa.2020.102138
DO - 10.1016/j.plefa.2020.102138
M3 - Article
C2 - 32663656
AN - SCOPUS:85087720763
SN - 0952-3278
VL - 159
JO - Prostaglandins Leukotrienes and Essential Fatty Acids
JF - Prostaglandins Leukotrienes and Essential Fatty Acids
M1 - 102138
ER -