Development of intestinal adhesions prophylaxis after emergency surgery by IFN gamma- STAT1 -PAI-1 signal suppression
Development of intestinal adhesions prophylaxis after emergency surgery by IFN gamma- STAT1 -PAI-1 signal suppression
批准号:
23592679
负责人:
UEDA Kentaro
金额:
$2.58万
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
项目状态:
已结题
起止时间:
2011 至 2013
中文摘要
我们构建了特异性抑制STAT1的SOCS1表达载体和PAI-1 siRNA载体,并利用这些载体在小鼠肠道粘连模型中检测了粘连的预防作用。我们设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三组组织学黏附程度无差异,但D组、E组黏附程度有明显改善。我们发现骨髓、肝脏和肾脏在所有组中都没有副作用。
英文摘要
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.
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Development of the new radiation therapy using tumor suppressor gene NPRL2 for esophageal cancer
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批准号:20591575
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.25万
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财政年份:2008
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负责人:UEDA Kentaro
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依托单位: