Splenic Immune Cells in Experimental Neonatal Hypoxia–Ischemia

摘要: Neuroimmune processes contribute to hypoxic–ischemic damage in the immature brain and may play a role progression of particular variants neonatal encephalopathy. The present study was designed elucidate molecular mediators interactions between astrocytes, neurons, infiltrating peripheral immune cells after experimental hypoxia–ischemia (HI). Splenectomy performed on postnatal day 7 Sprague–Dawley rats 3 days prior HI surgery, which right common carotid artery permanently ligated followed by 2 h hypoxia (8 % O2). Quantitative analysis showed that natural killer (NK) T cell expression reduced spleen but increased following HI. Elevations cyclooxygenase-2 (COX-2) promoted interleukin-15 (IL-15) astrocytes infiltration inflammatory site injury; additionally, these downregulated prosurvival protein, phosphoinositide-3-kinase (PI3K), resulting caspase 3-mediated neuronal death. removal largest pool body splenectomy COX-2 inhibitors as well rendering NK inactive CD161 knockdown significantly ameliorated cerebral infarct volume at 72 h, diminished weight loss systemic organ atrophy, neurobehavioral deficits weeks. Herein, we demonstrate with use surgical approach (splenectomy) pharmacological loss–gain function using inhibitors/agonists cell-type-specific siRNA HI, modulate downstream targets death neuroinflammation COX-2-regulated signals.