Project/Area Number |
24590337
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
|
Research Institution | Kinki University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
NIWA Atsuko 近畿大学, 医学部, 講師 (60122082)
NISHIBORI Masahiro 岡山大学, 医歯薬総合研究科, 教授 (50135943)
RYU Katsuyaku 岡山大学, 医歯薬総合研究科, 助教 (40432637)
中村 恭子 近畿大学, 付置研究所, 助教 (10512197)
大島 佳奈 近畿大学, 医学部, 助手 (60278653)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | High mobility group box1 / SHR / 高血圧症 / 抗HMGB1抗体 / high mobility group box1 |
Outline of Final Research Achievements |
Recent studies have shown that high mobility group box1 (HMGB1) plays roles in immune response. We have reported that anti-HMGB1 Ab inhibited the progression of brain infarction and atherosclerosis. However, little is known whether HMGB1 induces the vascular injury, we investigated the involvement of HMGB1 in the endothelial dysfunction and injury using stroke-prone spontaneously hypertensive rats (SHRSP). It is well known that the endothelial dysfunction and injury induces hypertension. Although we could not prove the effect of HMGB1 on the endothelial dysfunction and injury, during this project, we found the mechanism of neutrophil-induced endothelial dysfunction and injury. Moreover, we found a mediator which inhibited the activation of neutrophil. Therefore, we continue the promotion of basic scientific research for formulating drugs for treatment of hypertension.
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