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J Neurosci Res. 1999 Jun 15;56(6):652-8.

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

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1
Department of Neurology, Baylor College of Medicine, Houston, Texas 77030, USA. Weidongl@bcm.tmc.edu

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.

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