Protective role of heme oxygenase-1 in oxidative stress-induced neuronal injury.

Abstract:

:Heme oxygenase-1 (HO-1) is a stress protein induced in response to a variety of oxidative challenges. After treatment of the hybrid septal cells SN 56 with beta-amyloid peptide (beta-AP1-40) or hydrogen peroxide (H2O2), we detected high levels of reactive oxygen species, accompanied by a significant elevation in HO-1 expression. Levels of HO-1 increased and then decreased following cell loss. Pretreatment of SN 56 cells with HO-1 antisense oligonucleotides dramatically decreased the immunoreactivity of HO-1 and significantly enhanced the cytotoxicity of beta-AP1-40 and H2O2. In contrast, pretreatment with hemin, an HO-1 inducer, increased the expression of HO-1 and decreased the beta-AP1-40- and H2O2-induced cytotoxicity. These findings support the importance of HO-1 in protecting neurons against oxidative stress-induced injury.

journal_name

J Neurosci Res

authors

Le WD,Xie WJ,Appel SH

doi

10.1002/(SICI)1097-4547(19990615)56:6<652::AID-JNR

keywords:

subject

Has Abstract

pub_date

1999-06-15 00:00:00

pages

652-8

issue

6

eissn

0360-4012

issn

1097-4547

pii

10.1002/(SICI)1097-4547(19990615)56:6<652::AID-JNR

journal_volume

56

pub_type

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