کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10958379 | 1100021 | 2010 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neuroprotective effects of salidroside against beta-amyloid-induced oxidative stress in SH-SY5Y human neuroblastoma cells
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کلمات کلیدی
DcfAβGAPDHDCFH-DAAPPAPAf-12′,7′-dichlorofluorescin - 2 '، 7'-dichlorofluorescin2′,7′-dichlorofluorescin diacetate - 2 '، 7'-dichlorofluorescin diacetateERK1/2 - ERK1 / 2extracellular signal-regulated kinase1/2 - kinase1 / 2 تنظیم شده سیگنال خارج سلولیethidium bromide - اتیدیوم برومایدBeta-amyloid - بتا آمیلوئیدAlzheimer's disease - بیماری آلزایمرantioxidant responsive element - عنصر پاسخ دهنده آنتی اکسیدانARE - هستندbeta-amyloid precursor protein - پروتئین پیش ساز بتا آمیلوئید
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Beta-amyloid (Aβ) peptide, the hallmark of Alzheimer's disease (AD), invokes a cascade of oxidative damages to neurons and eventually leads to neuronal death. In this study, salidroside (Sald), an active compound isolated from a traditional Chinese medicinal plant, Rhodiola rosea L., was investigated to assess its protective effects and the underlying mechanisms against Aβ-induced oxidative stress in SH-SY5Y human neuroblastoma cells. Aβ25-35-induced neuronal toxicity was characterized by the decrease of cell viability, the release of lactate dehydrogenase (LDH), morphological alterations, neuronal DNA condensation, and the cleavage of poly(ADP-ribose) polymerase (PARP) by activated caspase-3. Pretreatment with salidroside markedly attenuated Aβ25-35-induced loss of cell viability and apoptosis in a dose-dependent manner. The mechanisms of salidroside protected neurons from oxidative stress included the induction of antioxidant enzymes, thioredoxin (Trx), heme oxygenase-1 (HO-1), and peroxiredoxin-I (PrxI); the downregulation of pro-apoptotic protein Bax and the upregulation of anti-apoptotic protein Bcl-XL. Furthermore, salidroside dose-dependently restored Aβ25-35-induced loss of mitochondrial membrane potential (MMP) as well as suppressed the elevation of intracellular reactive oxygen species (ROS) level. It was also observed that Aβ25-35 stimulated the phosphorylation of mitogen-activated protein (MAP) kinases, including c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase, but not extracellular signal-regulated kinase1/2 (ERK1/2). Salidroside inhibited Aβ25-35-induced phosphorylation of JNK and p38 MAP kinase, but not ERK1/2. These results suggest that salidroside has protective effects against Aβ25-35-induced oxidative stress, which might be a potential therapeutic agent for treating or preventing neurodegenerative diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 57, Issue 5, November 2010, Pages 547-555
Journal: Neurochemistry International - Volume 57, Issue 5, November 2010, Pages 547-555
نویسندگان
Li Zhang, Huixin Yu, Xincan Zhao, Xiufeng Lin, Chen Tan, Guoxian Cao, Zhengwu Wang,