Approach to elucidate the pathogenesis of multiple organ disfunction syndrome in critically ill patients

阐明危重患者多器官功能障碍综合征发病机制的途径

• 批准号: 22592014
• 负责人: TABATA Takahisa
• 金额: $ 2.91万
• 依托单位: Shiga University of Medical Science
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22592014/
• 关键词: 多臓器不全; インスリン; 骨髄細胞; 多臟器不全; インスリン治療

On the aspect that the pathogenesis of multiple organ dysfunction syndromes (MODS) is resembles to that of end-stage diabetes mellitus (DM) patients, we investigated the mechanism of MODS by referring the results of recent advance of DM research. In patients who died by MODS, we found the proinsulin positive cells in both kidney and liver. These cells were also TNF-alpha positive in confocal study. These results suggest that the high glucose induces proinsulin positive cells in bone marrow, and those cells invade to visceral organs, release a TNF-alpha, and resulted in MODS.

鉴于多器官功能障碍综合征（MODS）的发病机制与终末期糖尿病（DM）患者的发病机制相似，我们参考DM研究的最新进展，探讨了MODS的发病机制。在死于 MODS 的患者中，我们在肾脏和肝脏中发现了胰岛素原阳性细胞。这些细胞在共聚焦研究中也呈 TNF-α 阳性。这些结果表明，高葡萄糖诱导骨髓中胰岛素原阳性细胞，这些细胞侵入内脏器官，释放TNF-α，导致MODS。