甘露糖结合凝集素途径是 2 型糖尿病心脏再灌注损伤的重要贡献者。
The mannose-binding lectin pathway is a significant contributor to reperfusion injury in the type 2 diabetic heart.
机构信息
Department of Surgery, University of Arizona, Tucson, AZ 85724-5071, USA.
出版信息
Diab Vasc Dis Res. 2009 Jul;6(3):172-80. doi: 10.1177/1479164109336051.
Abstract
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 FUT175 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.
摘要
2 型糖尿病显著加重缺血性心脏病的严重程度。我们最近报道称，补体激活会加剧 2 型糖尿病心脏的 I/R 损伤。本研究旨在分离并检测 I/R 损伤后 2 型糖尿病心脏中 MBL 途径的激活。ZLC 和 ZDF 大鼠接受 30 分钟的左冠状动脉闭塞，然后再灌注 120 分钟。对两组不同的 ZDF 大鼠分别用广谱补体抑制剂 FUT-175 和针对大鼠 MBL-A 的单克隆抗体 P2D5 进行处理。与未处理的 ZDF 对照组相比，用 FUT175 和 P2D5 处理的 ZDF 大鼠的心肌梗死面积、C3 沉积和中性粒细胞聚集明显减少。综上所述，这些发现表明 MBL 途径在 2 型糖尿病心脏中补体介导的 I/R 损伤的严重程度中起关键作用。
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本文引用的文献
1
Mannose-binding lectin plays a critical role in myocardial ischaemia and reperfusion injury in a mouse model of diabetes.
Diabetologia. 2008 Aug;51(8):1544-51. doi: 10.1007/s00125-008-1044-6. Epub 2008 May 21.
2
Whole blood aggregation and coagulation in db/db and ob/ob mouse models of type 2 diabetes.
Blood Coagul Fibrinolysis. 2008 Mar;19(2):124-34. doi: 10.1097/MBC.0b013e3282f41e56.
3
Complement inhibition reduces injury in the type 2 diabetic heart following ischemia and reperfusion.
Am J Physiol Heart Circ Physiol. 2008 Mar;294(3):H1282-90. doi: 10.1152/ajpheart.00843.2007. Epub 2008 Jan 4.
4
Fluorochrome-linked immunoassay for functional analysis of the mannose binding lectin complement pathway to the level of C3 cleavage.
J Immunol Methods. 2007 Jun 30;323(2):147-59. doi: 10.1016/j.jim.2007.04.004. Epub 2007 May 11.
5
C5aR-mediated myocardial ischemia/reperfusion injury.
Biochem Biophys Res Commun. 2007 Jun 1;357(2):446-52. doi: 10.1016/j.bbrc.2007.03.152. Epub 2007 Apr 2.
6
Increased platelet aggregation in vivo in the Zucker Diabetic Fatty rat: differences from the streptozotocin diabetic rat.
Br J Pharmacol. 2007 Jan;150(1):105-11. doi: 10.1038/sj.bjp.0706957. Epub 2006 Nov 13.
7
Complement activation and diabetic vascular complications.
Clin Chim Acta. 2005 Nov;361(1-2):10-9. doi: 10.1016/j.cccn.2005.04.028.
8
Mannose-binding lectin is a regulator of inflammation that accompanies myocardial ischemia and reperfusion injury.
J Immunol. 2005 Jul 1;175(1):541-6. doi: 10.4049/jimmunol.175.1.541.
9
Complement activation in diabetic ketoacidosis and its treatment.
Clin Immunol. 2005 Jul;116(1):11-7. doi: 10.1016/j.clim.2005.03.004.
10
Complement C3 is a risk factor for the development of diabetes: a population-based cohort study.
Diabetes. 2005 Feb;54(2):570-5. doi: 10.2337/diabetes.54.2.570.
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