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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.


Effect of arctigenin on HO-1 expression in rat primary astrocytes. Cells were treated with various concentration of arctigenin for 6 h (A, C) or incubated with 20 μM arctigenin for the indicated time points (B, D). The HO-1 protein and mRNA levels were determined by western blot and RT-PCR analyses. The data are representative of three independent experiments. Quantification data are shown at the bottom of each panel. Values are the mean ± S.E.M. of three independent experiments. *p<0.05, compared with the control group.
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f2-bt-22-497: Effect of arctigenin on HO-1 expression in rat primary astrocytes. Cells were treated with various concentration of arctigenin for 6 h (A, C) or incubated with 20 μM arctigenin for the indicated time points (B, D). The HO-1 protein and mRNA levels were determined by western blot and RT-PCR analyses. The data are representative of three independent experiments. Quantification data are shown at the bottom of each panel. Values are the mean ± S.E.M. of three independent experiments. *p<0.05, compared with the control group.

Mentions: To investigate the molecular mechanism underlying antioxidant effects of arctigenin, we examined the effect of arctigenin on the expression of HO-1, which plays a critical role as an antioxidant defense factor in the brain. Western blot and RTPCR analyses showed that arctigenin increased HO-1 expression at the protein and mRNA levels (Fig. 2). We observed that 5–20 μM of arctigenin upregulated HO-1 expression in a concentration-dependent manner (Fig. 2A, C). In addition, arctigenin (20 μM) induced HO-1 mRNA and protein expression at 1 h, the level of which was increased at least up to 6 h (Fig. 2B, D).


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)

Effect of arctigenin on HO-1 expression in rat primary astrocytes. Cells were treated with various concentration of arctigenin for 6 h (A, C) or incubated with 20 μM arctigenin for the indicated time points (B, D). The HO-1 protein and mRNA levels were determined by western blot and RT-PCR analyses. The data are representative of three independent experiments. Quantification data are shown at the bottom of each panel. Values are the mean ± S.E.M. of three independent experiments. *p<0.05, compared with the control group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f2-bt-22-497: Effect of arctigenin on HO-1 expression in rat primary astrocytes. Cells were treated with various concentration of arctigenin for 6 h (A, C) or incubated with 20 μM arctigenin for the indicated time points (B, D). The HO-1 protein and mRNA levels were determined by western blot and RT-PCR analyses. The data are representative of three independent experiments. Quantification data are shown at the bottom of each panel. Values are the mean ± S.E.M. of three independent experiments. *p<0.05, compared with the control group.
Mentions: To investigate the molecular mechanism underlying antioxidant effects of arctigenin, we examined the effect of arctigenin on the expression of HO-1, which plays a critical role as an antioxidant defense factor in the brain. Western blot and RTPCR analyses showed that arctigenin increased HO-1 expression at the protein and mRNA levels (Fig. 2). We observed that 5–20 μM of arctigenin upregulated HO-1 expression in a concentration-dependent manner (Fig. 2A, C). In addition, arctigenin (20 μM) induced HO-1 mRNA and protein expression at 1 h, the level of which was increased at least up to 6 h (Fig. 2B, D).

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.