Eicosanoid imbalance in the NOD mouse is related to a dysregulation in soluble epoxide hydrolase and 15-PGDH expression

被引：19

作者：

Rodriguez, Michelle ^{[1
]}

Clare-Salzler, Michael ^{[1
]}

机构：

[1] Univ Florida, Coll Med, Dept Pathol Immunol & Lab Med, Gainesville, FL 32610 USA

来源：

IMMUNOLOGY OF DIABETES IV: PROGRESS IN OUR UNDERSTANDING | 2006年 / 1079卷

关键词：

epoxide hydrolase; 15-PGDH; lipoxin A4; inflammation; type; 1; diabetes; eicosanoids;

D O I：

10.1196/annals.1375.019

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Eicosanoids promote or resolve inflammation depending on the class produced. Macrophage from nonobese diabetic (NOD) mouse produce increased proinflammatory lipid mediators and low levels of antiinflammatory lipoxin A4 (LXA4). The enhanced proinflammatory eicosanoids is secondary to increased cyclooxygenase-2 (Cox-2) expression and low levels of prostaglandin/leukotriene catabolic enzyme, 15-hydroxyprostaglandin dehydrogenase (15-PGDH). Deficient LXA4 production is not due to deficient lipoxygenase (LO) activity, but is related to increased soluble epoxide hydrolase (sEH), involved in metabolism of anti-inflammatory epoxyeicosatrienoic acids (EET). These aberrations in eicosanoid biology suggest that inflammation in the NOD mouse is likely to be prolonged and robust and may contribute to type I diabetes (T1D) pathogenesis.,

引用

页码：130 / 134

页数：5

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