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Neuroprotective effect of heme oxygenase-2 knockout in the blood injection model of intracerebral hemorrhage.

By Jing Chen-Roetling, Ying Cai and Raymond F Regan

Abstract

BACKGROUND: The toxicity of heme breakdown products may contribute to the pathogenesis of intracerebral hemorrhage (ICH). Heme catabolism is catalyzed by the heme oxygenase enzymes. We have previously reported that heme oxygenase-2 (HO-2), the constitutive isoform, protects neurons from hemin in vitro and reduces oxidative stress after striatal blood injection. In order to further evaluate HO-2 as a therapeutic target, we tested the hypothesis that HO-2 gene deletion protects neurons and attenuates behavioral deficits after ICH. FINDINGS: Injection of 20 μl blood into the right striatum of HO-2 wild-type mice resulted in loss of approximately one third of striatal neurons 4-8 days later. Neuronal survival was significantly increased in HO-2 knockout mice at both time points. This was associated with reduced motor deficit as detected by the corner test; however, no differences were detected in spontaneous activity or the adhesive removal or elevated body swing tests. CONCLUSION: HO-2 knockout attenuates perihematomal neuron loss in the blood injection ICH model, but has a weak and variable effect on neurological outcome

Topics: Department of Emergency Medicine, Thomas Jefferson University, heme oxygenase-2, intracerebral hemorrhage, ICH, Emergency Medicine
Publisher: Jefferson Digital Commons
Year: 2014
OAI identifier: oai:jdc.jefferson.edu:emfp-1034

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