Journal
BRAIN
Volume 130, Issue -, Pages 1643-1652Publisher
OXFORD UNIV PRESS
DOI: 10.1093/brain/awm095
Keywords
antioxidants; blood; hemin; HO-1; reactive oxygen species
Categories
Funding
- NATIONAL CENTER FOR COMPLEMENTARY &ALTERNATIVE MEDICINE [R21AT001836, R21AT002113] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS046400] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R21AA014911] Funding Source: NIH RePORTER
- NCCIH NIH HHS [AT001836, R21 AT001836, AT002113, R21 AT001836-01A1, R21 AT002113-01, R21 AT002113] Funding Source: Medline
- NIAAA NIH HHS [R21 AA014911, R21 AA014911-02, AA014911] Funding Source: Medline
- NINDS NIH HHS [R01 NS046400-03, NS046400, R01 NS046400] Funding Source: Medline
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Because heme oxygenase (HO) is the rate limiting enzyme in the degradation of the pro-oxidant hemin/heme from blood, here we investigated the contribution of the inducible HO-I to early brain injury produced by intracerebral haemorrhage (ICH). We found that after induction of ICH, IHO- I proteins were highly detectable in the peri-ICH region predominantly in microglia/macrophages and endlothelial cells. Remarkably, the injury volume was significantly smaller in IH10- I knockout (HO-I-/-) mice than in wild-type controls 24 and 72 h after ICH. Although the brain water content did not appear to be significantly different, the protection in HO-I-/- mice was associated with a marked reduction in ICH-induced leucocyte infiltration, microglia/macrophage activation and free radical levels.These data reveal a previously unrecognized role of HO- I in early brain injury after ICH.Thus, modulation of HO-I signalling should be assessed further in clinical settings, especially for haemorrhagic states.
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