Elucidation of the role of bioactive lipids in neuropathic pain
Project/Area Number |
23592276
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
|
Research Institution | The University of Tokyo |
Principal Investigator |
ITO NOBUKO 東京大学, 医学部附属病院, 講師 (80332609)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 脂質 / 炎症 / 疼痛学 / 神経科学 |
Research Abstract |
Leukotriene B4 (LTB4) is a potent lipid mediator enhancing recruitment and activation of neutrophils, which is a common feature of inflammation and tissue injury. We examined the involvement of LTB4 in acute pain models using LTB4 receptor (BLT1) deficiency mice. We found that BLT1 deletion reduced formalin-induced pain behaviors, peripheral inflammation and activations of Cyclic AMP-responsive element binding protein (CREB) in the dorsal horn. Activation of CREB in the spinal cord in response to peripheral noxious stimulation is known as an initial important step for central sensitization. Pretreatments of BLT1 antagonist were also effective for formalin-induced pain behaviors. LTB4-BLT1 signaling may contribute to not only peripheral inflammation but also the sensitization of nociceptors during persistent pain. The involvement of LTB4-BLT1 signaling is a key component of pain mechanisms and a powerful target for therapeutic intervention for acute and persistent pain state.
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Report
(4 results)
Research Products
(7 results)