کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6282006 1615130 2014 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Exogenous fractalkine enhances proliferation of endothelial cells, promotes migration of endothelial progenitor cells and improves neurological deficits in a rat model of ischemic stroke
ترجمه فارسی عنوان
فراتلکال اگزوژن موجب افزایش تکثیر سلولهای اندوتلیال می شود، باعث افزایش مهاجرت سلول های پیش گیاه اندوتلیال می شود و نقص عصبی را در یک مدل رت از سکته ایسکمیک بهبود می بخشد
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
چکیده انگلیسی
Fractalkine/CX3CL1, also called neurotactin, has been described as an angiogenic agent, and its expression is up-regulated in the penumbra after ischemia. This study was conducted to investigate the neovascular potential of fractalkine on rat models of transient middle cerebral artery occlusion (MCAO). Rats receiving intracerebroventricular injections of fractalkine were found to have improved neurological deficits, reduced cerebral infarct size and increased neuron survival for both doses (100 ng and 1 μg). Fractalkine exerted angiogenic effects that showed dose-dependent higher vascular densities in the peri-infarct area. Furthermore, exogenous fractalkine increased the proliferation of endothelial cells in a dose-dependent manner and enhanced the migration of endothelial progenitor cells at the higher dose (1 μg) in ischemic penumbra. In conclusion, intracerebroventricular administration of fractalkine reduces ischemic damage by promoting neuroprotection and by inducing endothelial cell proliferation and endothelial progenitor cell migration, thereby enhancing neovascularization in the peri-infarct region.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 569, 21 May 2014, Pages 80-84
نویسندگان
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