Abstract:
:Heme oxygenase-1 (HO1) catalyzes oxidation of the heme molecule in concert with NADPH-cytochrome P450 reductase following the specific cleavage of heme into carbon monoxide, iron, and biliverdin, which is rapidly metabolized to bilirubin. HO1 is a stress-inducible protein that protects cells against oxidative injury, but its protective mechanism is not fully understood. The Eizai hyperbilirubinemic rat (EHBR), a mutant strain derived from the Sprague-Dawley rat (SDR), has a mutation in the gene for the canalicular multispecific organic anion transporter, which results in a phenotype of hyperbilirubinemia, and thus is a model of Dubin-Johnson syndrome in humans. In this study, we compared EHBR and SDR with regard to neuronal death induced by 2 hr of occlusion of the middle cerebral artery and reperfusion. In EHBR, the area that was immunoreactive for microtubule-associated protein-2 was significantly reduced, and the HO1-immunoreactive area was smaller than that in SDR. These results suggest that bilirubin has essentially a neuroprotective effect against focal ischemia and may participate in HO1-induced neuroprotection.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Kitamura Y,Ishida Y,Takata K,Mizutani H,Kakimura J,Inden M,Nakata J,Taniguchi T,Tsukahara T,Akaike A,Shimohama Sdoi
10.1002/jnr.10514keywords:
subject
Has Abstractpub_date
2003-02-15 00:00:00pages
544-50issue
4eissn
0360-4012issn
1097-4547journal_volume
71pub_type
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