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Synergistic induction of heme oxygenase-1 by nicaraven after subarachnoid
hemorrhage to prevent delayed cerebral vasospasm.

Shimada Y, Tsunoda H, Zang L, Hirano M, Oka T, Tanaka T.

Cerebral vasospasm remains a major cause of morbidity and mortality in patients
with subarachnoid hemorrhage. Heme oxigenase-1 (HO-1) is an oxidative
stress-inducible enzyme with multiple protective functions against vascular and
neurological diseases, including delayed cerebral vasospasm. In the present
study, intravenous administration (i.v.) of nicaraven (1mg/kg/min, for 2days
after subarachnoid hemorrhage) ameliorated delayed cerebral vasospasm in rat
subarachnoid hemorrhage models, marked synergistic induction of HO-1 protein
(>2.5 folds than 'subarachnoid hemorrhage with saline i.v.'), and elicited a
rapid increase of cGMP accumulation in the basilar arteries. In the sham-operated
rats, nicaraven could not induce HO-1 expression. Antisense HO-1
oligodeoxynucleotides abrogated this HO-1 induction and the antivasospastic
effect of nicaraven. In vitro study using Hela cells, nicaraven enhanced the
human HO-1 promoter (-4.5kbp) activity, which was pre-activated with the blood
component oxyhemoglobin to mimic the ability of subarachnoid hemorrhage. These
results suggest that this enhanced HO-1 expression through a combination of
pathological state and pharmacological agent could be an effective strategy to
improve the prognosis of heme- and oxidative stress-induced diseases, such as
delayed cerebral vasospasm.

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