Development of intestinal adhesions prophylaxis after emergency surgery by IFN gamma- STAT1 -PAI-1 signal suppression

通过干扰素γ-STAT1-PAI-1信号抑制预防急诊手术后肠粘连的进展

• 批准号: 23592679
• 负责人: UEDA Kentaro
• 金额: $ 2.58万
• 依托单位: Wakayama Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23592679/
• 关键词: マウス腸管癒着モデル; siPAI-1 HVJ vector; SOCS1 HVJ vector; HVJ Envelope vector; PAI-1 siRNA; SOCS1; 術後腸管癒着; PAI-1 SiRNA

We constructed SOCS1 expression vector to suppress STAT1 specifically and PAI-1 siRNA vector, and examined the prevention effect of adhesion in mouse intestinal adhesion model using these vectors.We had set the 5 group: A: Control group, B: SOCS1 group, C: PAI-1 siRNA group, D: SOCS1 + PAI-1 siRNA group, F: HGF (positive control). The results were equivalent to that of the F group was no difference in the three groups A, B, and C histology with the degree of adhesion, but adhesion is improved edge in the D group and E group. We found no side effects of bone marrow, liver, to the kidney in all groups.

我们构建了抑制STAT1和PAI-1 siRNA载体的SOCS1表达载体，并用这些载体在小鼠肠粘连模型中检测了其对粘连的预防作用。设置5组：A：对照组，B：SOCS1组，C：PAI-1 siRNA组，D：SOCS1+PAI-1 siRNA组，F：HGF(阳性对照)。结果与F组相当，A、B、C三组组织学上的粘连程度无差异，但D组和E组的边缘粘连有所改善。各组均未发现骨髓、肝脏、肾脏的副作用。