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

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

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


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.

Original languageEnglish (US)
Article number102138
JournalProstaglandins Leukotrienes and Essential Fatty Acids
StatePublished - Aug 2020
Externally publishedYes


  • Asphyxial cardiac arrest (ACA)
  • Cerebral ischemia
  • Hippocampus
  • Long chain saturated fatty acid
  • Neuroinflammation
  • Neuroprotection
  • Stearic acid methyl ester (SAME)

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology


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