Abstract
Microglia recover and maintain homeostasis in the central nervous system by phagocytosing dead cells and harmful substances under pathological conditions. Chemerin 15 (C15), a chemerin-derived peptide, is an endogenous phagocytic and inflammatory regulator that acts via the G protein-coupled receptor, ChemR23. However, the effect of C15 on microglial phagocytosis following ischemia-reperfusion injury remains unclear. Here, we found that microglial phagocytosis was activated and dynamically altered after ischemia-reperfusion injury. C15 administration promoted microglial phagocytosis of bioparticles and neuronal debris and upregulated the phagocytosis-related genes and pathways. Furthermore, C15 binding to ChemR23 decreased damage-associated molecular patterns (DAMPs) and ROS production and further alleviated the infarct volume and neurological deficits after ischemia-reperfusion injury. Thus, C15 is a potential therapeutic target for the recovery of neurological function after stroke.