ArticleBiomolecules & therapeutics2014
Arctigenin Increases Hemeoxygenase-1 Gene Expression by Modulating PI3K/AKT Signaling Pathway in Rat Primary Astrocytes.
Article in Biomolecules & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 22 citations in OpenAlex.
- Optimized New Shengmai Powder suppresses ferroptosis in ischemic cardiomyocytes via cGMP-PKG signalling.Chinese medicine · 2026Article
- Targeting the oxidative stress-neuroinflammation axis: the mechanism of arctigenin's broad-spectrum analgesia with limited side effects.Frontiers in immunology · 2026Article
- Arctigenin: pharmacology, total synthesis, and progress in structure modification.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Lignans as Pharmacological Agents in Disorders Related to Oxidative Stress and Inflammation: Chemical Synthesis Approaches and Biological Activities.International journal of molecular sciences · 2022Review
- Heme, Heme Oxygenase, and Endoplasmic Reticulum Stress-A New Insight into the Pathophysiology of Vascular Diseases.International journal of molecular sciences · 2019Review
- The antitumor function of arctigenin in human retinoblastoma cells is mediated by jagged‑1.Molecular medicine reports · 2019Article
- Arctigenin, a Potent Ingredient of Arctium lappa L., Induces Endothelial Nitric Oxide Synthase and Attenuates Subarachnoid Hemorrhage-Induced Vasospasm through PI3K/Akt Pathway in a Rat Model.BioMed research international · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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