Galangin Activates the ERK/AKT-Driven Nrf2 Signaling Pathway to Increase the Level of Reduced Glutathione in Human Keratinocytes
Biomolecules & Therapeutics
;
: 427-433, 2017.
Article
in English
| WPRIM
| ID: wpr-147982
ABSTRACT
Previously, we demonstrated that galangin (3,5,7-trihydroxyflavone) protects human keratinocytes against ultraviolet B (UVB)-induced oxidative damage. In this study, we investigated the effect of galangin on induction of antioxidant enzymes involved in synthesis of reduced glutathione (GSH), and investigated the associated upstream signaling cascades. By activating nuclear factor-erythroid 2-related factor (Nrf2), galangin treatment significantly increased expression of glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione synthetase (GSS). This activation of Nrf2 depended on extracellular signal-regulated kinases (ERKs) and protein kinase B (AKT) signaling. Inhibition of GSH in galangin-treated cells attenuated the protective effect of galangin against the deleterious effects of UVB. Our results reveal that galangin protects human keratinocytes by activating ERK/AKT-Nrf2, leading to elevated expression of GSH-synthesizing enzymes.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Keratinocytes
/
Catalytic Domain
/
Extracellular Signal-Regulated MAP Kinases
/
Proto-Oncogene Proteins c-akt
/
Glutamate-Cysteine Ligase
/
Glutathione
/
Glutathione Synthase
Limits:
Humans
Language:
English
Journal:
Biomolecules & Therapeutics
Year:
2017
Type:
Article
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