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Stearic acid methyl ester affords neuroprotection and improves functional outcomes after cardiac arrest

2020; Elsevier BV; Volume: 159; Linguagem: Inglês

10.1016/j.plefa.2020.102138

1532-2823

Po-Yi Chen, Celeste Yin‐Chieh Wu, Garrett A. Clemons, Cristiane T. Citadin, Alexandre Couto e Silva, Harlee E. Possoit, Rinata Azizbayeva, Nathan E. Forren, Chin‐Hung Liu, K.N. Shashanka Rao, David M. Krzywanski, Reggie Hui‐Chao Lee, Jake T. Neumann, Hung Wen Lin,

S100 Proteins and Annexins

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.