書誌事項
- タイトル別名
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- TNF-α/actinomycin D-mediated HepG2 cells in the presence of iron as a model of hepatocyte injury
- テツ ソンザイ カ HepG2 サイボウ ニ オケル TNF-a/actinomycin D ショリ ニ ヨル カン ショウガイ モデル ノ コウチク
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抄録
We examained the contribution of iron to the cytotoxicity of tumor necrosis factor (TNF)-a combined with actinomycin D (ActD) as a model of hepatocyte injury in Hep G2 cells. In general,hepatocytes are resistant to TNF-a. However,a transcriptional inhibitor such as ActD can sensitize then to TNF-a. In the present study, we show that low levels of ActD (0.5nM) sensitized HepG2 cells to the cytotoxic effects of TNF-a (20 ng/mL) for 48h. Iron plays a critical role in catalyxing the formation of potent oxidants. To acsses the toxicological significance of this TNF-a/ActD interaction,ferric-nitrilotriacetate (Fe-NTA,2uM) was added to the cells. Treatment with Fe-NTA significantly increased the sensitivity to the TNF-a/ActD-mediated cell death. TNF-a/ActD-mediated cell death in the presence of a lower concentration of iron did not result in DNA fragmentation. We suggest that iron increased the sensitivity to the cytotoxicity of TNF-a/ActD in HepG2 cells. It is likely that TNF-a/ActD/Fe-NTA-mediated cell death contributes to the non-apoptotic death of cells via oxidative stress caused by iron. Our experimental model may be useful for studying hepatic drug metabolism using TNF-a as a hepatocyte injury,especially in HepG2 cells.
収録刊行物
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- 東北薬科大学研究誌
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東北薬科大学研究誌 (59), 69-74, 2012-12
仙台 : 東北薬科大学
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詳細情報 詳細情報について
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- CRID
- 1050282812579678848
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- NII論文ID
- 110009587971
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- NII書誌ID
- AA1149311X
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- ISSN
- 1345157X
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- NDL書誌ID
- 024738457
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- 本文言語コード
- ja
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- 資料種別
- departmental bulletin paper
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- データソース種別
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- IRDB
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