The treatment with a ligand of Transcriptional Factor improves sepsis survival through anti-inflammatory effects
转录因子配体治疗通过抗炎作用提高脓毒症患者的生存率
基本信息
- 批准号:18591979
- 负责人:
- 金额:$ 0.99万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2006
- 资助国家:日本
- 起止时间:2006 至 2007
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Objective: Septic shock is the most common cause of death in intensive care unit next to cardiovascular diseases. Unfortunately, no effective treatment for this condition currently exists. Peroxisome proliferator-activated receptor (PPAR)-_Yligands are reported to reduce inflammatory responses. To evaluate the hypothesis that PPAR-_Yligands improve survival of septic shock, a mouse model of sepsis (apolipoprotein E (ApoE) knockout) was used and treated with pioglitazone, a PPAR-_Yligand. ApoE knockout mice have high mortality rate in sepsis due to lack of endotoxin clearance. Design and settings; Prospective laboratory study in a university laboratory. Subjects: Total 72 male ApoE knock out mice and 60 wild type C57/B6 mice randomized into three groups (sepsis, pre-treatment, post-treatment). Interventions; Cecal ligation and puncture were done in the sepsis and treatment groups. Mice injected with pioglitazone (5mg/kg/day) on the day before operation or mice injected with pioglitazone 6 hours after operation. Measurements and Main Results: Both pre- and post- operation treatment of pioglitazone improved survival of mortality in ApoE knock out and wild type mice. Serum levels of cytokines and chemokines, myeloperoxidase activity of lung and liver showed the same suppression in pioglitazone treatment group. Pioglitazone also suppressed monocytes adhesion to vascular endothelium under flow condition. Conclusions: Pioglitazone improved survival rate of apoE knockout mice after onset of septic shock through suppression of inflammatory respon
目的:感染性休克是重症监护病房中仅次于心血管疾病的最常见死亡原因。不幸的是,目前还没有有效的治疗方法。据报道过氧化物酶体增殖物激活受体(PPAR)-γ配体可减少炎症反应。为了评估PPAR-Y配体改善脓毒性休克存活率的假设,使用脓毒症小鼠模型(载脂蛋白E(ApoE)敲除)并用PPAR-Y配体吡格列酮治疗。ApoE基因敲除小鼠由于缺乏内毒素清除能力,在脓毒症中具有高死亡率。设计和设置;在大学实验室进行的前瞻性实验室研究。受试者:共72只雄性ApoE基因敲除小鼠和60只野生型C57/B6小鼠随机分为三组(脓毒症组、治疗前组、治疗后组)。干预:脓毒症组和治疗组进行盲肠结扎和穿刺。术前一天注射吡格列酮(5 mg/kg/天)或术后6 h注射吡格列酮。测量和主要结果:术前和术后吡格列酮治疗均改善了ApoE基因敲除小鼠和野生型小鼠的存活率和死亡率。吡格列酮治疗组血清细胞因子和趋化因子水平、肺和肝髓过氧化物酶活性均受到抑制。吡格列酮也抑制单核细胞粘附到血管内皮细胞在流动条件下。结论:吡格列酮通过抑制感染性休克后的炎症反应,提高apoE基因敲除小鼠的存活率。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Pioglitazone reduces systematic inflammation and improves mortality in apolipoprotein E knockout mice with sepsis
- DOI:10.1007/s00134-008-1024-9
- 发表时间:2008-07-01
- 期刊:
- 影响因子:38.9
- 作者:Haraguchi, Go;Kosuge, Hisanori;Isobe, Mitsuaki
- 通讯作者:Isobe, Mitsuaki
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ISOBE Mitsuaki其他文献
ISOBE Mitsuaki的其他文献
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{{ truncateString('ISOBE Mitsuaki', 18)}}的其他基金
Exploring the novel compounds targeting dysregulated autophagy-mediated cardiac dysfunction
探索针对自噬失调介导的心功能障碍的新型化合物
- 批准号:
15H04817 - 财政年份:2015
- 资助金额:
$ 0.99万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Development of new treatment for atherosclerosis by regulating cell-mediated immunity
通过调节细胞介导的免疫开发动脉粥样硬化新疗法
- 批准号:
20590880 - 财政年份:2008
- 资助金额:
$ 0.99万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Analysis of molecular mechanism of immunological rejection of transplanted heart and development of gene therapy for heart rejection
移植心脏免疫排斥的分子机制分析及心脏排斥基因治疗的进展
- 批准号:
14370221 - 财政年份:2002
- 资助金额:
$ 0.99万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Pathophysiological analysis and gene therapy of thoracic and abdominal aortic aneurysm
胸腹主动脉瘤的病理生理分析及基因治疗
- 批准号:
10470162 - 财政年份:1998
- 资助金额:
$ 0.99万 - 项目类别:
Grant-in-Aid for Scientific Research (B).
Treatment of Cardiac Diseases by Suppression of Cell Adhession
通过抑制细胞粘附治疗心脏病
- 批准号:
07457166 - 财政年份:1995
- 资助金额:
$ 0.99万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
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