RETRACTED: The Aminopyridinol Derivative BJ-1201 Protects Murine Hippocampal Cells against Glutamate-Induced Neurotoxicity via Heme Oxygenase-1 (Retracted Article. See vol 21, Art no 1463, 2016)open access
- Authors
- Lee, Dong-Sung; Nam, Tae-Gyu; Jeong, Byeong-Seon; Jeong, Gil-Saeng
- Issue Date
- May-2016
- Publisher
- MDPI AG
- Keywords
- aminopyridinol compound BJ-1201; neuroprotection; aminopyridinol HT22; heme oxygenase-1; nuclear transcription factor erythroid-2 related factor 2
- Citation
- MOLECULES, v.21, no.5, pp.1 - 11
- Indexed
- SCIE
SCOPUS
- Journal Title
- MOLECULES
- Volume
- 21
- Number
- 5
- Start Page
- 1
- End Page
- 11
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/14023
- DOI
- 10.3390/molecules21050594
- ISSN
- 1420-3049
- Abstract
- Glutamate is the major excitatory neurotransmitter in the brain. It can cause neuronal cell damage in the context of oxidative stress. BJ-1201 is a derivative of the compound aminopyridinol, which is known for its antioxidant activity. In this study, we examined the effect of BJ-1201, a 6-(diphenylamino)-2,4,5-trimethylpyridin-3-ol compound, on neuroprotection in HT22 cells. Our data showed that BJ-1201 can protect HT22 cells against glutamate-induced cell cytotoxicity. In addition, BJ-1201 upregulated heme oxygenase-1 (HO-1) to levels comparable to those of the CoPP-treated group. BJ-1201 treatment induced phosphorylation of JNK, but not p38-MAPK or ERK. It also increased the signal in the reporter assay based on beta-galactosidase activity driven by the nuclear transcription factor erythroid-2 related factor 2 (Nrf2) promoter harboring antioxidant response elements (AREs) and induced the translocation of Nrf2. These results demonstrate that BJ-1201 may be a good therapeutic platform against neurodegenerative diseases induced by oxidative stress.
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