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首页> 外文期刊>International immunopharmacology >Captopril inhibits maturation of dendritic cells and maintains their tolerogenic property in atherosclerotic rats
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Captopril inhibits maturation of dendritic cells and maintains their tolerogenic property in atherosclerotic rats

机译：卡托普利抑制动脉粥样硬化大鼠的树突状细胞成熟并维持其致耐受性

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Atherosclerosis (AS) is a systemic disease of the immune system featuring hyperactive dendritic cells (DCs) in atherosclerotic plagues and organs. Captopril, a representative medicine of angiotensin-converting enzyme inhibitors, has been demonstrated to be effective in treating AS. However, captopril's anti-atherosclerotic mechanism is still poorly understood. Therefore, this study was primarily performed to investigate the effects of captopril on the function of DCs in vivo. AS in rats was induced by feeding them with atherogenic diets, and it was evaluated by the levels of plasma lipids and aortic cholesterol. DCs' activity was appraised by endocytic activity, mixed lymphocyte reactions and cytokine secretion. The markers of DCs (CD103, CD80, CD86 and MHC-II) and Treg (CD4(+), CD25(+) and Foxp(3+)) were assayed by western blotting analysis and flow cytometry. Cytokine level was measured by an enzyme-linked immunosorbent assay. The results showed that captopril treatment (10, 20 mg/kg/d) obviously improved dyslipidemia and reduced the levels of aortic cholesterol. Captopril significantly reduced CD103, CD80, CD86 and MHC-II protein expression while increasing that of Foxp3 in aortic tissue. Further study indicated oral administration of captopril up-regulated endocytic activity and reduced the immunostimulatory function of splenic DCs. Captopril treatment also promoted IL-10 & TGF-beta production while decreasing that of IL-6 & IL-12 in splenic DCs. Finally, the results of flow cytometry indicated that captopril obviously inhibited DC maturation and promoted Treg polarization. Captopril treatment was able to inhibit DC maturation and maintain their tolerogenic property, which is closely associated with DC anti-atherosclerosis activity. (C) 2015 Published by Elsevier B.V.
机译：动脉粥样硬化（AS）是一种免疫系统疾病，以动脉粥样硬化鼠疫和器官中的过度树突状细胞（DC）为特征。卡托普利是血管紧张素转化酶抑制剂的代表药物，已被证明可有效治疗AS。然而，卡托普利的抗动脉粥样硬化机制仍知之甚少。因此，本研究主要是为了研究卡托普利对体内DC功能的影响。通过给大鼠补充动脉粥样化饮食来诱导其产生AS，并通过血浆脂质和主动脉胆固醇水平对其进行评估。 DC的活性通过内吞活性，混合淋巴细胞反应和细胞因子分泌来评估。通过western印迹分析和流式细胞仪检测DCs（CD103，CD80，CD86和MHC-II）和Treg（CD4（+），CD25（+）和Foxp（3+））的标志物。通过酶联免疫吸附测定法测量细胞因子水平。结果表明，卡托普利治疗（10，20 mg / kg / d）可明显改善血脂异常，并降低主动脉胆固醇水平。卡托普利显着降低CD103，CD80，CD86和MHC-II蛋白表达，同时增加主动脉组织中Foxp3的表达。进一步的研究表明，口服卡托普利可上调内吞活性，并降低脾脏DC的免疫刺激功能。卡托普利治疗还促进了脾脏DC中IL-10和TGF-β的产生，同时降低了IL-6和IL-12的产生。最后，流式细胞术的结果表明卡托普利明显抑制DC成熟并促进Treg极化。卡托普利治疗能够抑制DC的成熟并维持其致耐受性，这与DC的抗动脉粥样硬化活性密切相关。 （C）2015由Elsevier B.V.发布

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