Carbon emission sources, emission factors, and references.

Carbon emission sources, emission factors, and references.</p

Results of the spatial convergence model of AGTFP in the YRD region.

Results of the spatial convergence model of AGTFP in the YRD region.</p

Average value of AGTFP and its decomposition in the YRD region from 2001 to 2019.

Average value of AGTFP and its decomposition in the YRD region from 2001 to 2019.</p

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

<div><p>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 A₂-IIA (sPLA₂-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 sPLA₂-IIA in neuroinflammation is more complicated and remains unclear yet. In the present study, we investigated the effect of sPLA₂-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 sPLA₂-IIA alleviated the release of PGE₂ by suppressing the activation of ERK1/2, cPLA₂α, COX-2 and mPGES-1. These findings demonstrated that sPLA₂-IIA showed the potential to regulate the neuroinflammation in vivo and in vitro, indicating that sPLA₂-IIA might be a novel target for the treatment of acute neuroinflammation.</p></div