کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6274295 | 1614821 | 2013 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hesperidin pretreatment protects hypoxia-ischemic brain injury in neonatal rat
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کلمات کلیدی
PFANeurobasalHIE2′,7′-dichlorodihydro-fluorescein diacetateFluoro-Jade BOGDFJBDCFH-DATTCDMEMDMSO - DMSODulbecco’s modified Eagle medium - Modified Eagle اصلاح شده DulbeccoMTT - MTTROS - ROSDIV - دیوDimethyl sulfoxide - دیمتیل سولفواکسیدdays in vitro - روز in vitronormal saline - سالین نرمالBlood–brain barrier - سد خونی مغزیBBB - سد خونی مغزیlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH Oxygen and glucose deprivation - محرومیت از اکسیژن و گلوکزHesperidin - هسپریدینparaformaldehyde - پارافرمالدهیدReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Neonatal hypoxia-ischemic encephalopathy (HIE) remains a major cause of brain damage, leading to high disability and mortality rates in neonates. In vitro studies have shown that hesperidin, a flavanone glycoside found abundantly in citrus fruits, acts as an antioxidant. Although hesperidin has been considered as a potential treatment for HIE, its effects have not been fully evaluated. In this study, the protective effect of hesperidin pretreatment against hypoxia-ischemic (HI) brain injury and possible signal pathways were investigated using in vivo and in vitro models. In vivo HI model employed unilateral carotid ligation in postnatal day 7 rat with exposure to 8% hypoxia for 2.5Â h, whereas in vitro model employed primary cortical neurons of neonatal rats subjected to oxygen and glucose deprivation for 2.5Â h. Hesperidin pretreatment significantly reduced HI-induced brain tissue loss and improved neurological outcomes as shown in 2,3,5-triphenyltetrazolium chloride monohydrate staining and foot-fault results. The neuroprotective effects of hesperidin are likely the results of preventing an increase in intracellular reactive oxygen species and lipid peroxide levels. Hesperidin treatment also activated a key survival signaling kinase, Akt, and suppressed the P-FoxO3 level. Hesperidin pretreatment protected neonatal HIE by reducing free radicals and activating phosphorylated Akt.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 255, 26 December 2013, Pages 292-299
Journal: Neuroscience - Volume 255, 26 December 2013, Pages 292-299
نویسندگان
Z. Rong, R. Pan, Y. Xu, C. Zhang, Y. Cao, D. Liu,