کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4345674 | 1296747 | 2010 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Salidroside attenuates hypoxia-induced abnormal processing of amyloid precursor protein by decreasing BACE1 expression in SH-SY5Y cells
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کلمات کلیدی
sAPPαAβAPPPEN-2HIF-1αβ-site APP cleaving enzymeanterior pharynx-defective 1BACEAph-1Presenilin enhancer 2HREADAM - آدامamyloid-beta - آمیلوئید بتاAlzheimer's disease - بیماری آلزایمرa disintegrin and metalloproteinase - تخریب و متالوپروتئینازSalidroside - سالیدروزیدhypoxia-inducible factor 1α - عامل القایی هیپوکسی 1αhypoxia response element - عنصر پاسخ هیپوکسیHypoxia - هیپوکسیPresenilin - پرنسیلینamyloid precursor protein - پروتئین پیش ماده آمیلوئی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Hypoxia which is mainly mediated by hypoxia-inducible factor 1 (HIF-1), can greatly contribute to the occurrence of Alzheimer's disease (AD) by increasing β-site APP cleaving enzyme (BACE1) gene expression, protein level and β-secretase activity, resulting in a significant generation of amyloid-beta (Aβ). Salidroside has been reported to have great neuroprotective effects. The aim of this study was to investigate the effects of salidroside on hypoxia-induced abnormal processing of the amyloid precursor protein (APP) in SH-SY5Y cells and its possible mechanism. Western blot analysis showed that 200 μM of salidroside pretreatment significantly decreased BACE1 protein level and promoted the secretion of sAPPα in hypoxic condition. Salidroside had no effect on the level of APP, ADAM10 and ADAM17. ELISA analysis revealed that salidroside was able to inhibit the increase of β-secretase activity and Aβ generation induced by hypoxia, with no effect on γ-secretase activity. Notably, under hypoxia condition, mRNA of BACE1 and protein level of HIF-1α were decreased by salidroside pretreatment. These results demonstrated for the first time that salidroside was able to attenuate abnormal processing of amyloid precursor protein induced by hypoxia in SH-SY5Y cells, providing a new insight into prevention and treatment of Alzheimer's disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 481, Issue 3, 13 September 2010, Pages 154-158
Journal: Neuroscience Letters - Volume 481, Issue 3, 13 September 2010, Pages 154-158
نویسندگان
Qing-Yun Li, Hong-Mei Wang, Zhi-Quan Wang, Jian-Fang Ma, Jian-Qing Ding, Sheng-Di Chen,