The Role of Kupffer Cells in Carbon Tetrachloride Intoxication in Mice
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- Kiso Kaori
- Department of Food Science and Nutrition, Nara Women’s University
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- Ueno Satoko
- Department of Food Science and Nutrition, Nara Women’s University
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- Fukuda Mana
- Department of Food Science and Nutrition, Nara Women’s University
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- Ichi Ikuyo
- Department of Food Science and Nutrition, Graduate School of Humanities and Science, Ochanomizu University
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- Kobayashi Keiko
- Department of Food Science and Nutrition, Nara Women’s University
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- Sakai Takashi
- The Institute for Enzyme Research, The University of Tokushima
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- Fukui Kiyoshi
- The Institute for Enzyme Research, The University of Tokushima
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- Kojo Shosuke
- Department of Food Science and Nutrition, Nara Women’s University The Open University of Japan
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抄録
Carbon tetrachloride (CCl4)-induced acute hepatitis is assumed to involve two phases. The initial phase, initiated within 2 h after CCl4 administration, involves the generation of reactive oxygen species. The second phase is assumed to start about 8 h subsequent to CCl4 administration and involves the oxidant-induced activation of Kupffer cells, which release various pro-inflammatory mediators such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). We investigated the role of Kupffer cells during CCl4 intoxication using Nucling-knockout mice (the KO group), in which the number of Kupffer cells is largely reduced. Plasma alanine transaminase and aspartate transaminase levels demonstrated that the liver necrosis during the second phase was significantly alleviated in the KO group compared with that in the wild-type mice (the WT group). Plasma TNF-α concentrations in the WT group significantly increased 24 h after CCl4 intoxication, whereas those in the KO group did not significantly increase. Plasma IL-6 levels also significantly increased in the WT group 24 h after CCl4 administration, but those in the KO group did not increase at any time point. These results indicated that excess reactions of Kupffer cells, once primed by oxidants, were involved in the exacerbation of oxidative stress and liver damage during the second phase of CCl4 intoxication.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 35 (6), 980-983, 2012
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
- 1390001204633436544
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- NII論文ID
- 120005494833
- 130001872185
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC38jgslCrtQ%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 023665731
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- PubMed
- 22687543
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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
- IRDB
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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