Fig. 2
From: Mechanisms of neuroinflammation in hydrocephalus after intraventricular hemorrhage: a review
Blood components release triggers neuroinflammation and contributes to subsequent hydrocephalus. Hemoglobin and its primary metabolite iron, peroxiredoxin 2, and thrombin can induce hydrocephalus via pro-inflammatory activated macrophages (red CD68 + cells)/resident microglia (blue CD68 + cells), epiplexus cells (OX6 +), and granulocytes (MPO +).. Blocking blood components’ activity curtails neuroinflammation and alleviates post-hemorrhagic hydrocephalus. Estrogen can exacerbate thrombin-mediated brain injury and aggravate hydrocephalus. HO-1/2, heme oxygenase; LCN2, lipocalin-2; MPO, myeloperoxidase; IBA-1, ionized calcium binding adaptor molecule 1; OX-6, major histocompatibility complex II expressed by epiplexus cells; Prx2, peroxiredoxin 2; PAR-1, protease-activated receptor-1; SCH79797, 3-N-cyclopropyl-7-[(4-propan-2-ylphenyl)methyl]pyrrolo[3,2-f]quinazoline-1,3-diamine;dihydrochloride