| Project/Area Number |
17390537
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Okayama University |
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Principal Investigator |
MIYAWAKI Takuya Okayama University, Graduate Shool of Medicine, Dentisry, and Pharmacertical Sciences, Departrment of Disabilities and Dental Sciences and Dental Anesthesiology, Professor (00219825)
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| Co-Investigator(Kenkyū-buntansha) |
MAEDA Shigeru Okayama University Hospital, Department of Dental Anesthesiology, Associate Professor (50253000)
SAKURAI Satoru Tokyo Dental College, Department of Dental Anesthesiology, Senior Assistant Professor (50225843)
ICHINOHE Tatsuya Tokyo Dental College, Department of Dental Anesthesiology, Professor (40184626)
KOHJITANI Atsushi Kagoshima University, Gradurte School of Medicine and Dentistiy, Departments of Dental Anesthesiology, Associate Professor (60304325)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥15,920,000 (Direct Cost: ¥15,200,000、Indirect Cost: ¥720,000)
Fiscal Year 2007: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2006: ¥4,600,000 (Direct Cost: ¥4,600,000)
Fiscal Year 2005: ¥8,200,000 (Direct Cost: ¥8,200,000)
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| Keywords | Dentistry / Pharmacology / Cytokine / Inflammation / Anesthetics |
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| Research Abstract |
Intravenous anesthetics have been reported to modulate cytokine responses, but the mechanism of action on inflammatory response remains unclear. The purpose of the present study was to investigate the mechanism of intravenous anesthetic's action on cytokine and inflammatory responses. We evaluated the effects of midazolam, a intravenous anesthetic, on LPS-induced cytokine (interleukin-6) response in human peripheral blood mononuclear cells, focusing on a cyclooxygenase (COX) pathway. In results, the effect of midazolam was inhibited by indomethacin, a non-selective COX inhibitor, and NS-398, a COX-2 selective inhibitor, but not by SC-560, a COX-1 selective inhibitor. Midazolam did not alter any prostaglandins (prostaglandin E2, prostaglandin D2, and prostaglandin F2) production, although GW9662, an antagonist of peroxisome proliferator-activated receptor γ (PPARγ), masked the effect of midazolam. The results suggest that midazolam modulates the LPS-induced cytokine response via a COX-2 pathway around PPARγ. Furthermore, we evaluated the inhibitory effect of midazolam and dexmedetomidine, another intravenous anesthetic, on carrageenin-induced inflammatory edema at injection site in the mouse paw in vivo. The results suggest that they have an anti-inflammatory potency in vivo.
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