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 β-amyloid peptide (β-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 β-AP1-40 and H2O2. In contrast, pretreatment with hemin, an HO-1 inducer, increased the expression of HO-1 and decreased the β-AP1-40- and H2O2-induced cytotoxicity. These findings support the importance of HO-1 in protecting neurons against oxidative stress-induced injury.
Original language | English (US) |
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Pages (from-to) | 652-658 |
Number of pages | 7 |
Journal | Journal of Neuroscience Research |
Volume | 56 |
Issue number | 6 |
DOIs | |
State | Published - Jun 15 1999 |
Keywords
- β-Amyloid
- Alzheimer's disease
- Antioxidant
- Hydrogen peroxide
ASJC Scopus subject areas
- General Neuroscience