A study of neutrophils on diagnosis of the severity in organ dysfunction and the cause of death following hemorrhagic shock

中性粒细胞诊断失血性休克器官功能障碍严重程度及死因的研究

• 批准号: 20590692
• 负责人: TANAKA Noriyuki
• 金额: $ 1.25万
• 依托单位: University of Occupational and Environmental Health, Japan
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20590692/
• 关键词: 社会医学; 法医学; ショック; サイトカイン; 出血性ショック; BUN; クレアチニン

The role of neutrophils was studied by quantitatively grading four groups of hemorrhaging rats, focused on the kidney, so-called shock organ. As the amount of bleeding increased, the initial activation of p38 mitogen activated protein kinase(MAPK) and the expression of proinflammatory cytokines, such as tumor necrosis factor(TNF)-α and interleukin(IL)-1β, were progressively enhanced. The severity of renal dysfunction, manifested by serum creatinine concentration, was well correlated with the degree of neutrophils accumulation in the kidney. The present results confirmed that the frequency of activated neutrophils recruited into the kidney might be a useful for morphological diagnosis on the severity of renal dysfunction and that the increase of initial p38 MAPK activation following hemorrhagic shock quantitatively enhanced the ensuing inflammatory renal dysfunction in response to the degree and the progression of hemorrhagic shock.

通过对四组出血大鼠进行定量分级来研究中性粒细胞的作用，重点关注肾脏，即所谓的休克器官。随着出血量的增加，p38丝裂原激活蛋白激酶（MAPK）的初始激活和促炎性蛋白的表达。肿瘤坏死因子（TNF）-α和白细胞介素（IL）-1β等细胞因子逐渐增强，与血清肌酐浓度表现的肾功能不全严重程度密切相关。目前的结果证实，招募到肾脏中的活化中性粒细胞的频率可能有助于肾功能不全严重程度的形态学诊断，并且定量失血性休克后初始 p38 MAPK 活化的增加。增强了随后的炎症性肾功能障碍对失血性休克的程度和进展的反应。

项目成果

A quantitative study of p38 mitogen activated protein kinase on renal dysfunction following hemorrhagic shock in rats.

p38 丝裂原激活蛋白激酶对大鼠失血性休克后肾功能障碍的定量研究。

• 期刊: The Journal of Trauma (in press)
• 作者: H Sato;T Tanaka;K Kasai;N Tanaka
• 通讯作者: N Tanaka

出血性ショック時の腎障害と炎症性サイトカインとの関連に関する検討

失血性休克时肾损伤与炎症细胞因子关系的研究

• 发表时间: 2010
• 作者: 阿部裕子;大島俊二;神田智正;長谷場健;大野曜吉;佐藤寛晃,笠井謙多郎,田中敏子,田中宣幸
• 通讯作者: 佐藤寛晃,笠井謙多郎,田中敏子,田中宣幸