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Protection of Hippocampal Neuronal Cells from Buthionine Sulfoximine‐induced Oxidative Stress by Food‐derived Phase 2 Detoxifying Enzyme Inducers
Author(s) -
Kim Jong-Sang,
Lim Ji Sun,
Seo Jiyeon,
Jung Chaelim,
Han Jung-Hwa,
Park In-Sil,
Kang Hye-ryung,
Kim Seong Soon
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.692.13
Subject(s) - buthionine sulfoximine , oxidative stress , glutathione , antioxidant , biochemistry , chemistry , glutathione reductase , reactive oxygen species , pharmacology , enzyme , biology , glutathione peroxidase
The brain is sensitive to oxidative stress because it consumes a large amount of oxygen and has much polyunsaturated fatty acids. The dysfunction of the antioxidant/detoxification system may lead to neurodegenerative diseases such as Alzheimerˈs disease, Parkinsonˈs disease, and brain cerebral ischemia. Buthionine sulfoximine (BSO) is known to inhibit gamma‐GCS which is a precursor of glutathione. The imbalance of the oxidized/reduced forms of glutathione generates excessive reactive oxygen species and leads to oxidative stress in neuronal cells. Phytochemicals, present in a variety of plants, have numerous bioactive effects such as anticancer, anti‐inflammatory, and antioxidant activities. We hypothesized that phase 2 enzyme inducers protect neuronal cells from BSO‐induced oxidative damage. In order to test the hypothesis, HT22 neuronal cells pretreated with the known phase 2 enzyme inducers including dehydroglyasperin C (DGC) and acerogenin A was exposed to BSO. We also examined whether the expression of the antioxidant/phase 2 detoxifying enzymes is mediated by the nuclear translocation of Nrf2. DGC and acerogenin A were found to protect the neuronal cells from BSO‐induced toxicity, probably due to the induction of antioxidant enzymes such as heme oxygenase1 (HO‐1), glutathione reductase (GR), and NAD(P)H:quinone oxidoreductase 1 (NQO1) which, in turn, was mediated by Nrf2 signaling pathway.