The mannose-binding lectin pathway is a significant contributor to reperfusion injury in the type 2 diabetic heart

被引：23
作者：
La Bonte, Laura R. [2 ,3 ]
Dokken, Betsy [2 ,3 ]
Davis-Gorman, Grace [1 ,3 ]
Stahl, Gregory L. [4 ]
McDonagh, Paul F. [1 ,2 ,3 ]
机构：
[1] Univ Arizona, Dept Surg, Tucson, AZ 85724 USA
[2] Univ Arizona, Physiol Sci Grad Interdisciplinary Program, Tucson, AZ 85724 USA
[3] Univ Arizona, Sarver Heart Ctr, Tucson, AZ 85724 USA
[4] Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury, Dept Anesthesiol Perioperat & Pain Med,Sch Med, Cambridge, MA 02138 USA
来源：
DIABETES & VASCULAR DISEASE RESEARCH | 2009年 / 6卷 / 03期
关键词：
complement; Zucker Diabetic Fatty rat; inflammation; ischaemia-reperfusion injury; ENHANCES LEUKOCYTE ACCUMULATION; TERMINAL COMPLEMENT COMPONENTS; ACYLATION-STIMULATING PROTEIN; MEMBRANE ATTACK COMPLEX; MYOCARDIAL-ISCHEMIA; VASCULAR COMPLICATIONS; ISCHEMIA/REPERFUSION INJURY; CORONARY MICROCIRCULATION; CARDIOVASCULAR-DISEASE; ENDOTHELIAL-CELLS;
D O I：
10.1177/1479164109336051
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
The severity of ischaemic heart disease is markedly enhanced in type 2 diabetes. We recently reported that complement activation exacerbates I/R injury in the type 2 diabetic heart. The purpose of this study was to isolate and examine MBL pathway activation following I/R injury in the diabetic heart. ZLC and ZDF rats underwent 30 minutes of left coronary artery occlusion followed by 120 minutes of reperfusion. Two different groups of ZDF rats were treated with either FUT-175, a broad complement inhibitor, or P2D5, a monoclonal antibody raised against rat MBL-A. ZDF rats treated with FUT 175 and P2D5 had significantly decreased myocardial infarct size, C3 deposition and neutrophil accumulation compared with untreated ZDF controls. Taken together, these findings indicate that the MBL pathway plays a key role in the severity of complement-mediated I/R injury in the type 2 diabetic heart.
引用
收藏
页码：172 / 180
页数：9
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