Arctigenin increases hemeoxygenase-1 gene expression by modulating PI3K/AKT signaling pathway in rat primary astrocytes

Yeon Hui Jeong, Jin Sun Park, Dong Hyun Kim, Hee Sun Kim

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

In the present study, we found that the natural compound arctigenin inhibited hydrogen peroxide-induced reactive oxygen species (ROS) production in rat primary astrocytes. Since hemeoxygenase-1 (HO-1) plays a critical role as an antioxidant defense factor in the brain, we examined the effect of arctigenin on HO-1 expression in rat primary astrocytes. We found that arctigenin increased HO-1 mRNA and protein levels. Arctigenin also increases the nuclear translocation and DNA binding of Nrf2/c-Jun to the antioxidant response element (ARE) on HO-1 promoter. In addition, arctigenin increased ARE-mediated transcriptional activities in rat primary astrocytes. Further mechanistic studies revealed that arctigenin increased the phosphorylation of AKT, a downstream substrate of phosphatidylinositol 3-kinase (PI3K). Treatment of cells with a PI3K-specific inhibitor, LY294002, suppressed the HO-1 expression, Nrf2 DNA binding and ARE-mediated transcriptional activities in arctigenin-treated astrocyte cells. The results collectively suggest that PI3K/AKT signaling pathway is at least partly involved in HO-1 expression by arctigenin via modulation of Nrf2/ARE axis in rat primary astrocytes.

Original languageEnglish
Pages (from-to)497-502
Number of pages6
JournalBiomolecules and Therapeutics
Volume22
Issue number6
DOIs
StatePublished - 1 Nov 2014

Keywords

  • Arctigenin
  • Astrocyte
  • Hemeoxygenase-1
  • Nrf2/ARE axis
  • PI3K/AKT

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