徳島大学 教育・研究者情報データベース(EDB)

1. (英) Huang Huiwei

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2. (英) He Jianghong

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3. (英) Yuan Ying

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4. (英) Aoyagi Eriko

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5. (英) Takenaka Hidetaka

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6. (英) Itagaki Tatuzo

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7. (英) Sannomiya Katsutaka

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8. 玉木 克佳

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9. (英) Harada Nagakatsu

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10. 庄野 正行([徳島大学.大学院医歯薬学研究部.医学域.総合研究支援センター])

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11. 清水 一郎

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12. 高山 哲治([徳島大学.大学院医歯薬学研究部.医学域.医科学部門.内科系.消化器内科学])

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(英) Opposing effects of estradiol and progesterone on the oxidative stress-induced production of chemokine and proinflammatory cytokines in murine peritoneal macrophages.

(英) In inflammatory and oxidative liver injury, virus proteins and reactive oxygen species are involved in the regulation of proinflammatory cytokine production by macrophages. This study investigated the effects of estradiol (E2) and progesterone on the unstimulated and oxidative stress-stimulated production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, macrophage inflammatory protein (MIP)-2, and macrophage chemotactic protein (MCP)-1 by peritoneal macrophages isolated from male and female mice. E2 inhibited the cytokine production of TNF-alpha, IL-1beta, MIP-2, and MCP-1 by the unstimulated macrophages from males and females, which was then further stimulated by progesterone. The exposure to hydrogen peroxide in the macrophages from both sexes induced the production of cytokine. The hydrogen peroxide-stimulated cytokine production was suppressed by E2 and enhanced by progesterone. The sex hormone effects on the unstimulated and stimulated macrophages were blocked by their receptor antagonists and showed no significant difference between male and female subjects. These findings suggest that E2 may play a favorable role in the course of persistent liver injury, by inhibiting proinflammatory cytokine production, which, in addition, progesterone may counteract the favorable E2 effects through their receptors.

1. (英) Animals
2. (英) Cells, Cultured
3. (英) Chemokines
4. 細胞質分裂(cytokinesis)
5. (英) Depression, Chemical
6. (英) Estradiol
7. (英) Female
8. (英) Inflammation
9. (英) Inflammation Mediators
10. (英) Macrophages, Peritoneal
11. (英) Male
12. (英) Mice
13. (英) Mice, Inbred C3H
14. 酸化ストレス(oxidative stress)
15. (英) Progesterone
16. (英) Stimulation, Chemical

1. (英) Article.Affiliation: Department of Digestive and Cardiovascular Medicine, The University of Tokushima Graduate School, Tokushima, Japan.

2. (英) Article.PublicationTypeList.PublicationType: Journal Article