Microglia plays an important role in the production of inflammation in the central nervous system. Excessive nerve inflammation can cause neuronal damage and neurodegenerative disease. It has been shown that EPA-enriched ethanolamine plasmalogen (EPA-PlsEtn) significantly inhibited the expressions of inflammatory factors and suppressed neuronal loss in a rat model of Alzheimer's disease. However, whether EPA-PlsEtn protects against neuronal loss by inhibiting the activation of microglia is still not clear. Therefore, we examined the effect of PlsEtn on SH-SY5Y cells incubated by conditioned medium from LPS-induced BV2 cells as a neuroinflammation model. Results showed that pre-incubation of LPS-induced BV2 cells with PlsEtn significantly improved the viability of SH-SY5Y cells by reducing the early apoptosis. The increasing production of NO and TNF-α in BV2 cells was reversed by PlsEtn treatment, while the decreasing level of IL-10 was raised. Polarization toward M1 phenotype and activation of NLRP3 inflammasome pathways are attenuated significantly by pre-treatment of PlsEtn in LPS-induced BV2 cells. The study provides evidence for a positive effect of PlsEtn on neuroprotection and the inhibition of neuroinflammation, and PlsEtn may be explored as a potential functional ingredient with neuroprotection effects.
Keywords: EPA; Neuroinflammation; Neuroprotection; Phospholipids; Plasmalogen.
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