Project/Area Number |
24592321
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
|
Research Institution | University of Occupational and Environmental Health, Japan |
Principal Investigator |
KAWASAKI Chika 産業医科大学, 医学部, 非常勤医師 (60258621)
|
Co-Investigator(Kenkyū-buntansha) |
KAWASAKI Takashi 産業医科大学, 医学部, 准教授 (60299633)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 熱射病 / 中枢神経系 / ミクログリア / 炎症反応 / 中枢神経障害 / 炎症メディエーター / 熱中症 / 中枢神経 / 炎症性メディエーター |
Outline of Final Research Achievements |
The purpose of this study was to investigate the role of microglia on the inflammatory response of the brain in experimental heat stroke. After heat stress, the plasma and brain inflammatory mediators (TNF-alpha, IL-6, and HMGB1) levels were determined using ELISA. In control group(CG), plasma and brain TNF-alpha and IL-6 increased significantly at 2 hr after heat stress. Plasma and brain HMGB1 levels also increased in CG at 2 hr after heat stress. In minocycline treatment group(TG), these inflammatory responses ware suppressed compared to CG. Minocycline treatment decreased brain inflammatory responses, but plasma inflammatory mediators levels were not altered. This study demonstrated that minocycline suppressed brain inflammatory mediators concentrations after heat stress. Minocycline may be a beneficial treatment for heat stroke patients for down-regulating microglial cell-mediated inflammatory responses.
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