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The effects of ethanol on angiogenesis after myocardial infarction, and preservation of angiogenesis with rosuvastatin after heavy drinking

机译:乙醇对心肌梗死后血管生成的影响,并在重饮中血清楸的血管生成的保存

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The cardioprotective effects of moderate alcohol consumption and statins have been known for years. However, heavy or binge drinking confers a high risk of cardiovascular disease. This study aimed to investigate the effects of different levels of alcohol consumption on acute myocardial infarction that was induced experimentally in rats, with a focus on the potential mechanism of angiogenesis and the effects of statins on heavy drinking. The experimental rats were fed low-dose ethanol (0.5 g/kg/day), high-dose ethanol (5 g/kg/day), and high-dose ethanol with rosuvastatin (10 mg/kg/day) during the entire experiment. Acute myocardial infarctions were induced 4 weeks after the beginning of the experiment. We assessed the capillary density in the myocardium via immunohistochemistry and quantified the expression of vascular endothelial growth factor (VEGF) and endostatin via enzyme-linked immunosorbent assay kits on the 4th day after myocardial infarction. The results revealed that low ethanol consumption promoted angiogenesis in association with higher VEGF and lower endostatin. High ethanol intake suppressed angiogenesis with unchanged VEGF and elevated endostatin. Treatment with rosuvastatin preserved angiogenesis following high ethanol intake, with an upregulation of VEGF. This study highlights that low ethanol consumption obviously promotes angiogenesis in myocardial-infarction rats while increasing the expression of VEGF, whereas high ethanol consumption inhibits ischemia-induced angiogenesis. This study also provides evidence that rosuvastatin alleviates the inhibitory effects of heavy drinking on angiogenesis. (C) 2016 Elsevier Inc. All rights reserved.
机译:多年来已知中等酒精消费和他汀类药物的心脏保护作用。然而,重或狂暴饮用赋予了心血管疾病的高风险。本研究旨在探讨不同醇消耗水平对大鼠诱导的急性心肌梗死的影响,重点是血管生成的潜在机制及他汀类药物对重饮中的影响。将实验大鼠送入低剂量乙醇(0.5g / kg /天),高剂量乙醇(5g / kg / day),以及在整个实验期间用罗苏伐他汀(10mg / kg /天)的高剂量乙醇。在实验开始后4周诱导急性心肌梗塞。我们通过免疫组织化学评估了心肌中的毛细血管密度,并通过酶联免疫吸附测定试剂盒量化了血管内皮生长因子(VEGF)和内抑素的表达,在心肌梗死后第4天通过酶联免疫吸附试剂盒。结果表明,低乙醇消耗促进了与较高VEGF和下胚胎素相关的血管生成。高乙醇摄入量抑制了VEGF和升高的内皮素抑制血管生成。用高乙醇摄入后的血管生成的血管生成治疗,VEGF的上调。本研究突出显示低乙醇消耗明显促进心肌梗死大鼠的血管生成,同时增加VEGF的表达,而高乙醇消耗抑制缺血诱导的血管生成。本研究还提供了证据表明,罗苏伐他汀可减轻重饮料对血管生成的抑制作用。 (c)2016年Elsevier Inc.保留所有权利。

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