| Project/Area Number |
08671907
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | OITA MEDICAL UNIVERSITY |
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Principal Investigator |
NARAHARA Hisashi ASSOCIATE PROFESSOR OF DEPARTMENT OF OBSTETRICS AND GYNECOLOGY, OITA MEDICAL UNIVERSITY, 医学部, 助教授 (60211447)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUI Naohiko INSTRUCTOR OF DEPARTMENT OF OBSTETRICS AND GYNECOLOGY, OITA MEDICAL UNIVERSITY, 医学部, 助手 (00264341)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1998: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1997: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1996: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | platelet-activating factor / parturition / preterm labor / decidua / macrophages / cytokine / estrogen / endotoxin / プロゲステロン / 分娩発来 / プロテインキナーゼC / エンドセリン |
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| Research Abstract |
Platelet-activating factor(PAF), a potent lipid mediator, has been implicated in a number of reproductive processes, including parturition. PAF has been shown to stimulate prostaglandin EィイD22ィエD2 production in fetal membranes and to cause myometrial contraction. PAF metabolism in the decidua and its modulation by endotoxin or cytokines has been investigated. Decidual macrophages secrete PAF-acetylhydrolase (PAF-AH) activity of the plasma type that inactivates PAF. LPS, TNF-α, and IL-1β inhibited the PAF-AH secretion by decidual macrophages. The LPS-inhibition was partially reversed by IL-1ra or by neutralizing antibodies against TNF-α and IL-1β. The effect of IL-1β on the secretion was abolished by IL-1ra. IFN-γ, IL-6, and IL-8 also inhibited the PAF-AH secretion, while M-CSF increased the enzyme secretion. Estradiol inhibited the enzyme secretion, while progesterone stimulated the secretion. Endothelins decreased the PAF-AH secretion by decidual macrophages. These observations lend additional support to the concept that PAF is pathophysiologically involved in parturition or preterm labor caused by chorioamnionitis, forming a PAF-medeated cytokine network at the fetal-maternal decidual interface.
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