2-decenoic acid ethyl ester, a compound that elicits neurotrophin-like intracellular signals, facilitating functional recovery from cerebral infarction in mice.

In our previous study, we found that trans-2-decenoic acid ethyl ester (DAEE), a derivative of a medium-chain fatty acid, elicits neurotrophin-like signals including the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in cultured mouse cortical neurons. Here, we examined the efficacy of intraperitoneal administration of DAEE on the treatment of a mouse model of the cerebral infarction caused by unilateral permanent middle cerebral artery occlusion (PMCAO). DAEE-treatment (100 μg/kg body weight injected at 0.5, 24, 48, 72 h after PMCAO) significantly restored the mice from PMCAO-induced neurological deficits including motor paralysis when evaluated 48, 72, and 96 h after the PMCAO. Furthermore, DAEE facilitated the phosphorylation of ERK1/2 on the infarction side of the brain when analyzed by Western immunoblot analysis, and it enhanced the number of phosphorylated ERK1/2-positive cells in the border areas between the infarction and non-infarction regions of the cerebral cortex, as estimated immunohistochemically. As the infarct volume remained unchanged after DAEE-treatment, it is more likely that DAEE improved the neurological condition through enhanced neuronal functions of the remaining neurons in the damaged areas rather than by maintaining neuronal survival. These results suggest that DAEE has a neuro-protective effect on cerebral infarction.