RvD1binding with FPR2 attenuates inflammation via Rac1/NOX2 pathway after neonatal hypoxic-ischemic injury in rats.

ABSTRACT: Neuroinflammation plays a crucial role in the pathological development after neonatal hypoxia-ischemia (HI). Resolvin D1 (RvD1), an agonist of formyl peptide receptor 2 (FPR2), has been shown to exert anti-inflammatory effects in many diseases. The objective of this study was to explore the protective role of RvD1 through reducing inflammation after HI and to study the contribution of Ras-related C3 botulinum toxin substrate 1 (Rac1)/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) pathways in RvD1-mediated protection. Rat pups (10-day old) were subjected to HI or sham surgery. RvD1 was administrated by intraperitoneal injection 1 h after HI. FPR2 small interfering ribonucleic acid (siRNA) and Rac1 activation CRISPR were administered prior to RvD1 treatment to elucidate

SUBMITTER: Liu W 

PROVIDER: S-EPMC6708447 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature