Fiechter Danielle, Kats Suzanne, Brands Ruud, van Middelaar Ben, Pasterkamp Gerard, de Kleijn Dominique, Seinen Willem
Institute for Risk Assessment, University Utrecht, Utrecht, The Netherlands.
Department of Cardio-Thoracic Surgery, Maastricht University Medical Centre, Maastricht, The Netherlands.
Cardiol Res. 2011 Oct;2(5):236-242. doi: 10.4021/cr81w. Epub 2011 Sep 20.
There has been increasing evidence suggesting that lipopolysaccharide or endotoxin may be an important activator of the innate immune system after acute myocardial infarction. Bovine intestinal alkaline phosphatase reduces inflammation in several endotoxin mediated diseases by dephosphorylation of the lipid A moiety of lipopolysaccharide. The aim of this study was to investigate the effect of bovine intestinal alkaline phosphatase on reducing inflammation after acute myocardial infarction.
Just before permanent ligation of the left anterior descending coronary (LAD) artery to induce acute myocardial infarction in Balb/c mice, bovine intestinal alkaline phosphatase (bIAP) was administrated intravenously. After 4 hours, mice were sacrificed and the inflammatory response was assessed. Acute myocardial infarction induced the production of different cytokines, which were measured in blood.
Treatment with bovine intestinal alkaline phosphatase resulted in a significant reduction of the pro-inflammatory cytokines IL-6, IL-1β and the chymase mouse mast cell protease-1. No difference in the production of the anti-inflammatory cytokine IL-10 was observed between the control group and the bovine intestinal alkaline phosphatase treated group.
In a mouse model of permanent LAD coronary artery ligation, bIAP diminishes the pro-inflammatory responses but does not have an effect on the anti-inflammatory response in the acute phase after acute myocardial infarction.
越来越多的证据表明,脂多糖或内毒素可能是急性心肌梗死后先天性免疫系统的重要激活剂。牛小肠碱性磷酸酶通过使脂多糖的脂质A部分去磷酸化,减轻几种内毒素介导疾病中的炎症。本研究的目的是探讨牛小肠碱性磷酸酶对减轻急性心肌梗死后炎症的作用。
在对Balb/c小鼠进行左冠状动脉前降支(LAD)永久性结扎以诱导急性心肌梗死之前,静脉注射牛小肠碱性磷酸酶(bIAP)。4小时后,处死小鼠并评估炎症反应。急性心肌梗死诱导了不同细胞因子的产生,对血液中的细胞因子进行了检测。
牛小肠碱性磷酸酶治疗导致促炎细胞因子IL-6、IL-1β和糜酶小鼠肥大细胞蛋白酶-1显著减少。对照组和牛小肠碱性磷酸酶治疗组之间抗炎细胞因子IL-10的产生没有差异。
在永久性结扎LAD冠状动脉的小鼠模型中,bIAP可减轻急性心肌梗死后急性期的促炎反应,但对抗炎反应没有影响。