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首页> 外文期刊>Circulation journal >Sustained Release of Prostaglandin Ei Potentiates the ImpairedTherapeutic Angiogenesis by Basic Fibroblast Growth Factorin Diabetic Murine Hindlimb Ischemia
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Sustained Release of Prostaglandin Ei Potentiates the ImpairedTherapeutic Angiogenesis by Basic Fibroblast Growth Factorin Diabetic Murine Hindlimb Ischemia

机译：前列腺素Ei的持续释放增强了碱性成纤维细胞生长因子对糖尿病小鼠后肢缺血的治疗性血管生成的损害。

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Background Basic fibroblast growth factor bFGF is a potent mitogen; however, diabetes mellitus might impair its angiogenic property. Prostaglandin E1 PGE1 is a potent vasodilator and improves endothelial function. Thus, PGEi could potentiate the angiogenic properties of bFGF in patients with diabetes mellitus. Methods and Results Streptozotocin-induced diabetic mice with unilateral hindlimb ischemia were randomly treated as follows: no treatment, 0.2,ug of PGE1, lOjug of bFGF, and combined administration of PGEi and bFGF. Blood perfusion was evaluated by the ratio of ischemic- to normal-limb blood perfusion. Four weeks after the treatment, the combined administration of bFGF and PGEi increased the blood perfusion ratio as compared with single bFGF or PGEi 77+-10% vs 56+-10% and 58+-10%; p<0.05, respectively. A histological evaluation showed that vascular density in the combined therapy was higher than single bFGF or PGEi 418+-59 vs 306+-69 and 283+-71 vessels/mm2; p<0.01, respectively; the maturity in combined therapy was also higher than single bFGF or PGEi 46+-14 vs 30+14 and 28+-6 vessels/mm2; p<0.01, respectively.Conclusions PGE1 potentiated the impaired angiogenic properties of bFGF in diabetic murine hindlimb ischemia. This new strategy might contribute to more effective therapeutic angiogenesis for ischemic limb in patients with diabetes.
机译：背景碱性成纤维细胞生长因子bFGF是有效的促有丝分裂剂。但是，糖尿病可能会损害其血管生成特性。前列腺素E1 PGE1是有效的血管扩张剂，可改善内皮功能。因此，PGEi可以增强bFGF在糖尿病患者中的血管生成特性。方法和结果随机治疗链脲佐菌素诱导的糖尿病小鼠，方法如下：不治疗，0.2ug PGE1、10ug bFGF以及联合给药PGEi和bFGF。通过缺血与正常肢体血液灌注的比率评估血液灌注。治疗后四周，bFGF和PGEi的联合给药与单bFGF或PGEi相比增加了血液灌注率77 + -10％vs 56 + -10％和58 + -10％。 p ＜0.05。组织学评估表明，联合治疗中的血管密度高于单个bFGF或PGEi 418 + -59相对于306 + -69和283 + -71血管/ mm2; p分别为<0.01;联合疗法的成熟度也高于单bFGF或PGEi 46 + -14对比30 + 14和28 + -6血管/ mm2; p <0.01。结论PGE1在糖尿病鼠后肢缺血中增强了bFGF的血管生成特性。这种新的策略可能有助于糖尿病患者缺血肢体更有效的治疗性血管生成。

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