Elucidation of the role of inflammation-activated lipid signaling in incisional pain
| Project/Area Number |
26462377
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Anesthesiology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Ito Nobuko 東京大学, 医学部附属病院, 講師 (80332609)
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| Co-Investigator(Kenkyū-buntansha) |
浅原 美保 東京大学, 医学部附属病院, 助教 (60529155)
山田 芳嗣 東京大学, 医学部附属病院, 教授 (30166748)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 脂質 / 疼痛学 / 術後痛 / 疼痛 / 神経科学 |
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| Outline of Final Research Achievements |
We studied the involvement of Leukotriene B4 (LTB4) which is a potent neutrophil activator, in acute incisional pain model using high affinity LTB4 receptor (BLT1) deficiency mice. Mechanical nociceptive responses were reduced significantly on day2, day3 and day4 after incision in BLT1 deficiency mice compare to the wild type mice. Invasions of neutrophil were reduced significantly on day1 in BLT1 deficiency mice. Productions of TNF-alpha in incisional site were also reduced significantly on day1 in BLT1 deficiency mice. It was found that LTB4 that is produced as a lipid mediator at local site, induce the neutrophil invasion and cytokine production through its receptor BLT1 and contribute to acute incisional pain response.
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Report
(4 results)
Research Products
(9 results)
