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实验性糖尿病中前列环素的释放:月见草油的作用

Prostacyclin release in experimental diabetes: effects of evening primrose oil.

作者信息

Stevens E J, Carrington A L, Tomlinson D R

机构信息

William Harvey Research Institute, London, UK.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 1993 Sep;49(3):699-706. doi: 10.1016/0952-3278(93)90081-7.

Abstract

Alterations in release of endothelium-derived vasomotor agents could underlie microvascular and neuropathic complications in diabetes. This study examined release of the potent vasodilator prostacyclin, measured as immunoreactive 6-keto prostaglandin F1 alpha, from rat lung, kidney and peripheral nerve. Tissues were taken from control and streptozotocin-diabetic rats which had been treated for 8 weeks with either evening primrose oil (EPO) or, as a control for lipid intake, coconut oil (CO). Lung and kidney slices were incubated in the presence of acetylcholine (ACh), the calcium ionophore 4-Br-A23187, arachidonic acid (AA) or without agonist (basal). Segments of sciatic nerve, with their epineuria punctured, were incubated with or without 4-Br-A23187. Basal prostacyclin release from the lung was significantly higher in rats treated with EPO irrespective of diabetic state (increased by 60% in controls and by 77% in diabetics). Levels were reduced in CO-diabetics compared to EPO-controls (53% reduction) and CO-controls (30% reduction), although this did not reach statistical significance in the latter. Basal prostacyclin release was also significantly reduced in the kidney from CO-diabetics (40% reduction compared to CO-controls and 56% reduction compared to EPO-controls). In the presence of AA, lung prostacyclin release was significantly lower in CO-diabetic rats compared to all other groups (40% reduction compared to EPO-diabetics and 60% compared to both control groups) but there were no differences in renal release between any group. Prostacyclin release by nerves from CO-diabetic rats was significantly reduced (by 91-93%) compared to all other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

内皮源性血管舒缩因子释放的改变可能是糖尿病微血管和神经病变的基础。本研究检测了大鼠肺、肾和外周神经中强效血管舒张剂前列环素的释放情况,以免疫反应性6-酮前列腺素F1α进行测量。组织取自对照大鼠和经链脲佐菌素诱导的糖尿病大鼠,这些大鼠用月见草油(EPO)或作为脂质摄入对照的椰子油(CO)治疗8周。肺和肾切片在乙酰胆碱(ACh)、钙离子载体4-溴-A23187、花生四烯酸(AA)存在的情况下孵育,或在无激动剂(基础状态)下孵育。坐骨神经段,其神经外膜被刺破,在有或无4-溴-A23187的情况下孵育。无论糖尿病状态如何,用EPO治疗的大鼠肺组织基础前列环素释放均显著升高(对照组升高60%,糖尿病组升高77%)。与EPO对照组相比,CO治疗的糖尿病大鼠水平降低(降低53%),与CO对照组相比也降低(降低30%),尽管后者未达到统计学意义。CO治疗的糖尿病大鼠肾组织基础前列环素释放也显著降低(与CO对照组相比降低40%,与EPO对照组相比降低56%)。在AA存在的情况下,与所有其他组相比,CO治疗的糖尿病大鼠肺组织前列环素释放显著降低(与EPO治疗的糖尿病大鼠相比降低40%,与两个对照组相比降低60%),但各组肾组织释放无差异。与所有其他组相比,CO治疗的糖尿病大鼠神经组织前列环素释放显著降低(降低91%-93%)。(摘要截短至250字)

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