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Neuroinflammation is involved in various central nervous system (CNS) disorders, including brain infections, ischemia, trauma, stroke, and degenerative CNS diseases. In the CNS inflammation, secretory phospholipase A 2 -IIA (sPLA 2 -IIA) acts as a mediator, resulting in the generation of the precursors of pro-inflammatory lipid mediators, such as prostaglandins (PGs) and leukotrienes (LTs). However, the role of sPLA 2 -IIA in neuroinflammation is more complicated and remains unclear yet. In the present study, we investigated the effect of sPLA 2 -IIA inhibition by specific inhibitor SC-215 on the inflammation in LPS-induced mice cerebral cortex and primary astrocytes. Our results showed that the inhibition of sPLA 2 -IIA alleviated the release of PGE 2  by suppressing the activation of ERK1/2, cPLA 2 α, COX-2 and mPGES-1. These findings demonstrated that sPLA 2 -IIA showed the potential to regulate the neuroinflammation in vivo and in vitro, indicating that sPLA 2 -IIA might be a novel target for the treatment of acute neuroinflammation.

Inhibition of sPLA2-IIA Prevents LPS-Induced Neuroinflammation by Suppressing ERK1/2-cPLA2α Pathway in Mice Cerebral Cortex