PPARγ agonist rosiglitazone attenuates the development of neuropathic pain by regulating macrophage activation.
| Project/Area Number |
21791476
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Juntendo University |
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Principal Investigator |
TAKAHASHI Yoshika Juntendo University, 医学部, 助手 (70445550)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 慢性神経因性疼痛 / マクロファージ / PPARγ / Rosiglitazone / 炎症 / 補体受容体 / 神経再生 / ミクログリア |
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| Research Abstract |
Neuroinflammation triggered by macrophage infiltration into sites of peripheral nerve injury may result in neuropathic pain. Peroxisome proliferator-activated receptor gamma(PPARγ) signaling regulates the properties of macrophages. So we investigated the macrophage-mediated effects of PPARγ signaling on neuropathic pain triggered by peripheral inflammation using have not been partial sciatic nerve ligation (PSNL) mice model. PPARγ treatment in the early phase of neuropathic pain significantly alleviated the development of tactile allodynia by regulating macrophage infiltration and production of proinflammatory molecules at the inflamed site. Our results indicate that the activation of PPARγ signaling in macrophages during the early phase may suppress neuropathic pain development.
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Report
(3 results)
Research Products
(5 results)
