An active part of Artemisia sacrorum Ledeb. suppresses gluconeogenesis through AMPK mediated GSK3β and CREB phosphorylation in human HepG2 cells
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- YUAN Hai-Dan
- Department of Pharmacognosy, College of Pharmacy, Yan Bian University Department of Pharmacological Science, College of Pharmacy, Kyunghee University
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- PIAO Guang-Chun
- Department of Pharmacognosy, College of Pharmacy, Yan Bian University
書誌事項
- タイトル別名
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- An Active Part of Artemisia sacrorum Ledeb. Suppresses Gluconeogenesis through AMPK Mediated GSK3.BETA. and CREB Phosphorylation in Human HepG2 Cells
- An active part of Artemisia sacrorum Ledeb suppresses gluconeogenesis through AMPK mediated GSK3 v and CREB phosphorylation in human HepG2 cells
- An Active Part of<i>Artemisia sacrorum</i>Ledeb. Suppresses Gluconeogenesis through AMPK Mediated GSK3β and CREB Phosphorylation in Human HepG2 Cells
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抄録
In this study, we investigated the effects of a petroleum ether fraction of Artemisia sacrorum Ledeb. (Compositae) (PEASL) on glucose production through AMP-activated protein kinase (AMPK) activation in human HepG2 cells. PEASL significantly inhibited glucose production in a concentration-dependent manner, and this effect was reversed in the presence of compound C, a selective AMPK inhibitor. PEASL markedly induced the phosphorylation of AMPK and downstream acetyl-CoA carboxylase (ACC) in a time- and concentration-dependent manner. In addition, it markedly increased the phosphorylations of glycogen synthase kinase 3β (GSK3β) in a concentration-dependent manner. In contrast, cAMP reponse element binding protein (CREB), a key transcription factor for gluconeogenic enzyme phosphorylation, decreased in a concentration-dependent manner. PEASL downregulated the gluconeogenesis gene expression of peroxisome proliferation activated receptor-γ coactivator-1α (PGC-1α), phosphoenolpyruvate carboxykinase (PEPCK), and glucose-6-phosphatase (G6Pase) in a concentration-dependent manner. In addition, the gene expression of orphan nuclear receptor small heterodimer partner (SHP) increased, also in a concentration-dependent manner. These effects were also abolished by pretreatment with compound C, an AMPK inhibitor. This indicates that PEASL inhibited glucose production via the AMPK-GSK-CREB pathway in HepG2 cells, and these effects appeared to be capable of revealing anti-diabetic mechanism of PEASL in HepG2 cells.
収録刊行物
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- Bioscience, Biotechnology, and Biochemistry
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Bioscience, Biotechnology, and Biochemistry 75 (6), 1079-1084, 2011
公益社団法人 日本農芸化学会
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詳細情報 詳細情報について
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- CRID
- 1390001206478198272
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- NII論文ID
- 10029327928
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- NII書誌ID
- AA10824164
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- ISSN
- 13476947
- 09168451
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- NDL書誌ID
- 11131918
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可