کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4343956 | 1615144 | 2013 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Chitosan oligosaccharides protect rat primary hippocampal neurons from oligomeric β-amyloid 1-42-induced neurotoxicity
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کلمات کلیدی
DCFH-DAMDACOSSAβ42NFTsHFIPAPPAβCCK-8JnkSPS1,1,1,3,3,3-hexafluoro-2-propanol - 1،1،1،3،3،3-هگزافلوئورو 2-پروپانول2′,7′-dichlorofluorescin diacetate - 2 '، 7'-dichlorofluorescin diacetatec-Jun N-terminal kinase - C-Jun N-terminal kinaseMAPK - MAPKROS - ROSChitosan oligosaccharides - الیگوساکاریدها ChitosanAlzheimer's disease - بیماری آلزایمرNeurotoxicity - سمیت عصبیcell counting kit-8 - شمارش سلول کیت 8senile plaques - صفحات سالخوردهlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH malondialdehyde - مالون دی آلدهیدneurofibrillary tangles - مگس های نوروفیبریلیالamyloid precursor protein - پروتئین پیش ماده آمیلوئیmitogen activated protein kinase - پروتئین کیناز فعال Mitogen فعال استβ-amyloid peptide - پپتید β-آمیلوئیدReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
β-Amyloid peptide (Aβ), the major component of senile plaques in patients with Alzheimer's disease (AD), is believed to facilitate the progressive neurodegeneration that occurs in this disease. Mounting natural compounds are proved to be potential candidates for the prevention and treatment of AD. Chitosan oligosaccharides (COSs), the enzymatic hydrolysates of chitosan, have been reported to possess diverse biological activities. Here we investigated the effect of COSs on oligomeric Aβ-mediated toxicity in rat primary hippocampal neurons. Pretreatment with COSs markedly inhibited cell death induced by Aβ exposure as determined by cell viability assay and lactate dehydrogenase release assay. In parallel, the generation of reactive oxygen species and lipid peroxidation were attenuated by COSs. Furthermore, our results indicated that COSs remarkably prevented Aβ-induced cell apoptosis as manifested by depressing the elevation of Bax/Bcl-2 ratio and caspase-3 activation, suggesting that the neuroprotective effect of COSs could be partially due to apoptosis regulation. In addition, pretreatment with COSs significantly blocked Aβ-induced phosphorylation of c-Jun N-terminal kinase. Taken together, these findings may shed light on the role of COSs as a potential therapeutic agent for AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 554, 25 October 2013, Pages 64-69
Journal: Neuroscience Letters - Volume 554, 25 October 2013, Pages 64-69
نویسندگان
Xueling Dai, Ping Chang, Qingzhu Zhu, Wenjuan Liu, Yaxuan Sun, Shigong Zhu, Zhaofeng Jiang,