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Arctigenin Increases Hemeoxygenase-1 Gene Expression by Modulating PI3K/AKT Signaling Pathway in Rat Primary Astrocytes.

Jeong YH, Park JS, Kim DH, Kim HS - Biomol Ther (Seoul) (2014)

Bottom Line: In the present study, we found that the natural compound arctigenin inhibited hydrogen peroxide-induced reactive oxygen species (ROS) production in rat primary astrocytes.We found that arctigenin increased HO-1 mRNA and protein levels.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Medicine, Tissue Injury Defense Research Center, Ewha Womans University Medical School, Seoul 158-710.

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.

No MeSH data available.


Antioxidant effects of arctigenin in rat primary astrocytes. (A) Chemical structure of arctigenin. (B) Rat primary astrocyte cells were treated with 5 to 50 μM arctigenin for 1 h, followed by treatment of H2O2 (500 μM) for 30 min. The intracellular ROS levels were then measured by the DCF-DA method as described in the Materials and Methods section. The data are expressed as the mean ± S.E.M. of three independent experiments. *p<0.05, significantly different from H2O2-treated samples. ‘ATG’ indicates arctigenin.
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f1-bt-22-497: Antioxidant effects of arctigenin in rat primary astrocytes. (A) Chemical structure of arctigenin. (B) Rat primary astrocyte cells were treated with 5 to 50 μM arctigenin for 1 h, followed by treatment of H2O2 (500 μM) for 30 min. The intracellular ROS levels were then measured by the DCF-DA method as described in the Materials and Methods section. The data are expressed as the mean ± S.E.M. of three independent experiments. *p<0.05, significantly different from H2O2-treated samples. ‘ATG’ indicates arctigenin.

Mentions: Arctigenin was purchased from Enzo Life Sciences (Farmingdale, NY, USA). The chemical structure of arctigenin is as shown in Fig. 1A. All reagents used for cell culture were purchased from Thermo Scientific (Fremont, CA, USA). Antibodies against HO-1, Nrf-2, c-Jun, and lamin A were purchased from Santa Cruz Biotechnology (Dallas, Texas, USA). Antibodies against phospho- or total forms of ERK, JNK, p38, and AKT were obtained from Cell Signaling Technology (Danvers, MA, USA). All reagent used for RT-PCR were purchased from Promega (Madison, WI, USA).


Arctigenin Increases Hemeoxygenase-1 Gene Expression by Modulating PI3K/AKT Signaling Pathway in Rat Primary Astrocytes.

Jeong YH, Park JS, Kim DH, Kim HS - Biomol Ther (Seoul) (2014)

Antioxidant effects of arctigenin in rat primary astrocytes. (A) Chemical structure of arctigenin. (B) Rat primary astrocyte cells were treated with 5 to 50 μM arctigenin for 1 h, followed by treatment of H2O2 (500 μM) for 30 min. The intracellular ROS levels were then measured by the DCF-DA method as described in the Materials and Methods section. The data are expressed as the mean ± S.E.M. of three independent experiments. *p<0.05, significantly different from H2O2-treated samples. ‘ATG’ indicates arctigenin.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4256028&req=5

f1-bt-22-497: Antioxidant effects of arctigenin in rat primary astrocytes. (A) Chemical structure of arctigenin. (B) Rat primary astrocyte cells were treated with 5 to 50 μM arctigenin for 1 h, followed by treatment of H2O2 (500 μM) for 30 min. The intracellular ROS levels were then measured by the DCF-DA method as described in the Materials and Methods section. The data are expressed as the mean ± S.E.M. of three independent experiments. *p<0.05, significantly different from H2O2-treated samples. ‘ATG’ indicates arctigenin.
Mentions: Arctigenin was purchased from Enzo Life Sciences (Farmingdale, NY, USA). The chemical structure of arctigenin is as shown in Fig. 1A. All reagents used for cell culture were purchased from Thermo Scientific (Fremont, CA, USA). Antibodies against HO-1, Nrf-2, c-Jun, and lamin A were purchased from Santa Cruz Biotechnology (Dallas, Texas, USA). Antibodies against phospho- or total forms of ERK, JNK, p38, and AKT were obtained from Cell Signaling Technology (Danvers, MA, USA). All reagent used for RT-PCR were purchased from Promega (Madison, WI, USA).

Bottom Line: In the present study, we found that the natural compound arctigenin inhibited hydrogen peroxide-induced reactive oxygen species (ROS) production in rat primary astrocytes.We found that arctigenin increased HO-1 mRNA and protein levels.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Medicine, Tissue Injury Defense Research Center, Ewha Womans University Medical School, Seoul 158-710.

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.

No MeSH data available.