Antiinflammatory Effects of orientin 2"-O-Galactopyranoside on Lipopolysaccharide-Stimulated Microglia
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- Zhou Xiang
- Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University
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- Gan Ping
- Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University
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- Hao Lili
- Department of Traditional Chinese Medicine, College of Pharmaceutical Sciences, Soochow University
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- Tao Li
- Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University
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- Jia Jia
- Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University
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- Gao Bo
- Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University
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- Liu Jiang-yun
- Department of Traditional Chinese Medicine, College of Pharmaceutical Sciences, Soochow University
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- Zheng Long Tai
- Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University
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- Zhen Xuechu
- Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University
書誌事項
- タイトル別名
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- Antiinflammatory Effects of Orientin-2″-<i>O</i>-Galactopyranoside on Lipopolysaccharide-Stimulated Microglia
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説明
Microglia activation-mediated neuroinflammation plays an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and human immunodeficiency virus (HIV)-associated dementia. Inhibition of microglia activation may alleviate neurodegeneration under neuroinflammatory conditions. In the present study, we compared three flavone C-glycosides extracted from Trollius chinensis BUNGE using a cell-based assay to evaluate their antiinflammatory effects on microglial cells. The results showed that orientin-2″-O-galactopyranoside (OGA) significantly inhibited the production of nitric oxide and tumor necrosis factor (TNF)-α in lipopolysaccharide (LPS)-stimulated microglial cells. OGA also markedly inhibited the LPS-induced expression of TNF-α, interleukin-1β, inducible nitric oxide (NO) synthase, and cyclooxygenase-2, which was accompanied by suppression of the activation of nuclear factor (NF)-κB and the extracellular signal-regulated kinase (ERK) signal pathway. In addition, OGA decreased LPS-induced reactive oxygen species generation, which appears to be related to the activation of the NF-E2-related factor2 (NRF2)/ heme oxygenase-1 (HO-1) pathway in BV-2 microglial cells. Furthermore, OGA reduced the cytotoxicity of activated microglia toward HT-22 neuroblastoma cells in a co-culture system. Taken together, the present study demonstrated that the induction of HO-1-mediated inhibition of the NF-κB and ERK pathways contributes significantly to the antineuroinflammatory and neuroprotective effects elicited by OGA.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 37 (8), 1282-1294, 2014
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390282679608923904
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- NII論文ID
- 130004677534
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC2cbos1Kisg%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 025609849
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- PubMed
- 25087950
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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
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可