THE ROLE OF HMGB-1 AS CYTOKINE IN INFECTION
HMGB-1 作为细胞因子在感染中的作用
基本信息
- 批准号:15590397
- 负责人:
- 金额:$ 1.98万
- 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:2003
- 资助国家:日本
- 起止时间:2003 至 2004
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Lipopolysaccharide (LPS)-elicited chromogenic Limulus reaction was suppressed by pretreating LPS with a citrus flavonoid hesperidin (HES). Administration of HES to mice before LPS challenge significantly reduced tumor necrosis factor (TNF)-α production in a dose-dependent manner. Treatment of HES 3 h before intraperitoneal (i.p.) infection with 108 CFU Salmonella typhimurium aroA resulted in rescue from lethal shock as similar to LPS-nonresponder mice. Not only bacterial numbers in livers and spleens but also plasma LPS levels significantly decreased by pretreating with HES. In addition, HES markedly suppressed plasma TNF-a levels, decreased the number of apoptotic cells in livers and normalized the activated states of blood coagulation factors such as prothrombin time and platelet numbers caused by infection.The protective effect of Citrus flavanone naringin was demonstrated in an endotoxin shock model based on Salmonella infection. Intraperitoneal (i.p.) infection with 10^8 CFU Salmo … More nella typhimurium aroA caused lethal shock in lipopolysaccharide (LPS)-responder but not -nonresponder mice. Administration of 1 mg naringin 3 h before infection resulted in protection from lethal shock, similar to LPS-nonresponder mice. The protective effect of naringin was time- and dose-dependent. Treatment with naringin resulted not only in a significant decrease in bacterial numbers in spleens and livers, but also a decrease in plasma LPS levels. In addition, naringin markedly suppressed TNF-a and normalized the activated states of blood coagulation factors such as prothrombin time, fibrinogen concentration and platelet numbers caused by infection. Interestingly, treatment with naringin suppressed high levels of soluble CD14 and high mobility group-1 molecule caused by infection.The protective effects of an antibiotic polymyxin B (PLB), having lipopolysaccharide (LPS)-binding activity, on infection-induced endotoxin shock in mice were investigated. Infection with 10^8 colony forming units of an attenuated Salmonella typhimurium aroA strain caused lethal endotoxin shock to ddY mice. Treatment with PLB 1 h post infection (p.i.) resulted in significant reduction of mortality and bacterial numbers in livers. In addition, treatment with PLB 1 h p.i. resulted in a transient increase at the early stage and gradual decline in plasma LPS levels. Although plasma levels of sCD14 and high mobility group box chromosomal protein-1 (HMGB-1) increased according with progression of infection, increases in plasma levels of sCD14 and HMGB-1 were downregulated by treatment with PLB 1 h p.i. However, the lethal shock was not blocked by treatment with anti-CD14 monoclonal antibody at 3 h and 6 h p.i. Interestingly, administration of PLB 6 h p.i. did not show any protective activities, indicating that a time window for effective PLB action is present. Less
用柑橘类黄酮橙皮苷(HES)预处理脂多糖(LPS)可抑制LPS诱导的鲎显色反应。在LPS激发前给予小鼠HES,以剂量依赖性方式显著降低肿瘤坏死因子(TNF)-α的产生。腹膜内(i. p.)用108 CFU鼠伤寒沙门氏菌aroA感染导致从致死性休克中拯救,与LPS无应答小鼠相似。羟乙基淀粉预处理不仅能显著降低肝脏和脾脏中的细菌数量,而且能显著降低血浆中的LPS水平。此外,HES显著抑制血浆TNF-α水平,减少肝脏中凋亡细胞的数量,并使由感染引起的凝血因子如凝血酶原时间和血小板数量的活化状态正常化。腹膜内(i. p.)感染10^8 CFU萨尔莫 ...更多信息 鼠伤寒沙门氏菌aroA可引起脂多糖(LPS)应答小鼠的致死性休克,但对LPS无应答小鼠无影响。感染前3小时给予1 mg柚皮苷可保护小鼠免于致死性休克,与LPS无应答小鼠相似。柚皮苷的保护作用具有时间和剂量依赖性。柚苷治疗不仅导致脾脏和肝脏中细菌数量的显着减少,而且还降低了血浆LPS水平。此外,柚皮苷显着抑制TNF-α和正常化的凝血因子的活化状态,如凝血酶原时间,纤维蛋白原浓度和血小板数量引起的感染。有趣的是,柚苷治疗抑制高水平的可溶性CD 14和高迁移率族-1分子引起的infection. Polymyxin B(PLB),具有脂多糖(LPS)结合活性的抗生素的保护作用,对感染诱导的内毒素休克小鼠进行了研究。用10^8个菌落形成单位的减毒鼠伤寒沙门氏菌aroA菌株感染ddY小鼠,可引起致死性内毒素休克。感染后1小时(p.i.)导致死亡率和肝脏中细菌数量的显著降低。此外,用PLB处理lh p.i.导致血浆LPS水平在早期短暂升高并逐渐下降。尽管sCD 14和高迁移率族蛋白-1(HMGB-1)的血浆水平随着感染进展而升高,但PLB 1 h p.i.治疗可下调sCD 14和HMGB-1的血浆水平升高。然而,用抗CD 14单克隆抗体在感染后3小时和6小时处理不能阻断致死性休克。有趣的是,PLB 6 h p.i.没有显示出任何保护性活动,表明存在有效PLB行动的时间窗口。少
项目成果
期刊论文数量(9)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Kawaguchi K., Kikuchi S., Hasunuma R., et al.: "Suppression of Infection-Induced Endotoxin Shock in Mice by a Cifrus Flavanone Naringin"Planta Med.. 70・1. 17-22 (2004)
Kawaguchi K.、Kikuchi S.、Hasunuma R.等人:“柑橘黄酮柚皮苷对小鼠感染引起的内毒素休克的抑制”Planta Med.. 70・1 (2004)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Limitation of polymyxin B on suppression of endotoxin shock induced by Salmonella infection in mice.
多粘菌素 B 对抑制小鼠沙门氏菌感染引起的内毒素休克的限制。
- DOI:
- 发表时间:2004
- 期刊:
- 影响因子:0
- 作者:Morita;H.;R.Hasunuma;K.Kawaguchi et al.
- 通讯作者:K.Kawaguchi et al.
Kawaguchi K., Kikuchi S., Hasunuma R., et al.: "A Citrus Flavonoid Hesperidin Suppresses Infection-Induced Endotoxin Shock in Mice"Biol.Pharm.Bull.. 27・5(印刷中). (2004)
Kawaguchi K.、Kikuchi S.、Hasunuma R.等人:“柑橘类黄酮橙皮苷抑制小鼠感染引起的内毒素休克”Biol.Pharm.Bull.. 27・5(印刷中)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
A citrus flavonoid hesperidin suppresses infection-induced endotoxin shock in mice
- DOI:10.1248/bpb.27.679
- 发表时间:2004-05-01
- 期刊:
- 影响因子:2
- 作者:Kawaguchi, K;Kikuchi, S;Kumazawa, Y
- 通讯作者:Kumazawa, Y
Suppression of infection-induced endotoxin shock in mice by a Citrus flavanone naringin
- DOI:10.1055/s-2004-815449
- 发表时间:2004-01-01
- 期刊:
- 影响因子:2.7
- 作者:Kawaguchi, K;Kikuchi, S;Kumazawa, Y
- 通讯作者:Kumazawa, Y
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HASUNUMA Ryoichi其他文献
HASUNUMA Ryoichi的其他文献
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{{ truncateString('HASUNUMA Ryoichi', 18)}}的其他基金
ACTION MECHANISMS OF HMG-1 ON ENDOTOXIN SHOCK
HMG-1抗内毒素休克的作用机制
- 批准号:
13670282 - 财政年份:2001
- 资助金额:
$ 1.98万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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