Figure 3
From: von Willebrand factor contributes to poor outcome in a mouse model of intracerebral haemorrhage
VWF increased the expressions of cerebral inflammatory mediators after ICH.
(A–C) Relative gene expression of CXCL1, CX3CL1 and CCR1 in the brain of sham-operated mice and mice treated with vehicle or VWF 24 hours after ICH. (D–F) Quantification of MPO activity, IL-6 and IL-1β by ELISA in the brain of sham-operated mice and mice treated with vehicle or VWF 24 hours after ICH. Values are means ± standard errors of the means (n = 5). *P < 0.05. (G) LDH assay confirmed that the treatment of VWF did not induce cell death in cultured brain endothelial cells. Data are representative of 3 independent experiments. (H) Intraventricular injection of VWF did not show histological features of neuronal injury at 72 hours when examined with hematoxylin and eosin staining. (I) Intraventricular injection of VWF did not induce neurotoxic in normal mice at 72 hours when detected with TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling) staining. LV, lateral ventricle; CTX, cortex.
