کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6280433 | 1615095 | 2015 | 25 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Relationship between cerebral sodium-glucose transporter and hyperglycemia in cerebral ischemia
ترجمه فارسی عنوان
ارتباط بین حمل کننده سدیم گلوکز مغزی و هیپرگلیسمی در ایسکمی مغزی
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کلمات کلیدی
NDSα-MGPHZWST-8SGLTi.c.v.MCAOintracerebroventricularFBGTTC2,3,5-triphenyltetrazolium chloride - 2،3،5-trihenyltetrazolium chlorideHydrogen peroxide - آب اکسیژنهmiddle cerebral artery occlusion - انسداد شریان (سرخرگ) مغزی میانیFocal cerebral ischemia - ایسکمی مغز مرکزی کانونیANOVA - تحلیل واریانس Analysis of varianceone-way analysis of variance - تحلیل واریانس یک راههDIV - دیوday in vitro - روز in vitroCerebral stroke - سکته مغزیPhlorizin - فلویزینfasting blood glucose - قند خون ناشتاNeurological deficit score - نمره نارسایی عصبیprimary cortical neuron - نورون کورتنی اولیهHyperglycemia - هایپرگلایسمیH2O2 - هیدروژن پراکسید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Post-ischemic hyperglycemia exacerbates the development of cerebral ischemia. To elucidate this exacerbation mechanism, we focused on sodium-glucose transporter (SGLT) as a mediator that lead hyperglycemia to cerebral ischemia. SGLT transport glucose into the cell, together with sodium ion, using the sodium concentration gradient. We have previously reported that suppression of cerebral SGLT ameliorates cerebral ischemic neuronal damage. However, detail relationship cerebral between SGLT and post-ischemic hyperglycemia remain incompletely defined. Therefore, we examined the involvement of cerebral SGLT on cerebral ischemic neuronal damage with or without hyperglycemic condition. Cell survival rate of primary cultured neurons was assessed by biochemical assay. A mouse model of focal ischemia was generated using a middle cerebral artery occlusion (MCAO). Neuronal damage was assessed with histological and behavioral analyses. Concomitant hydrogen peroxide/glucose treatment exacerbated hydrogen peroxide alone-induced cell death. Although a SGLT family-specific inhibitor, phlorizin had no effect on developed hydrogen peroxide alone-induced cell death, it suppressed cell death induced by concomitant hydrogen peroxide/glucose treatment. α-MG induced a concentration-dependent and significant decrease in neuronal survival. PHZ administered on immediately after reperfusion had no effect, but PHZ given at 6 h after reperfusion had an effect. Our in vitro study indicates that SGLT is not involved in neuronal cell death in non-hyperglycemic condition. We have already reported that post-ischemic hyperglycemia begins to develop at 6 h after MCAO. Therefore, current our in vivo study show post-ischemic hyperglycemic condition may be necessary for the SGLT-mediated exacerbation of cerebral ischemic neuronal damage.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 604, 14 September 2015, Pages 134-139
Journal: Neuroscience Letters - Volume 604, 14 September 2015, Pages 134-139
نویسندگان
Yui Yamazaki, Shinichi Harada, Shogo Tokuyama,