کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10752101 | 1050322 | 2015 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Resolvin D2 recovers neural injury by suppressing inflammatory mediators expression in lipopolysaccharide-induced Parkinson's disease rat model
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کلمات کلیدی
Resolvin D2LPSIL-βTLR4MYD88NF-κBSNpc - SNPCinterleukin 1β - اینترلوکین 1βNeurodegenerative disease - بیماری های نوروژنیکParkinson's disease - بیماری پارکینسونsubstantia nigra pars compacta - توده سیاه پارس متراکمtumor necrosis factor α - تومور نکروز عامل αmyeloid differentiation factor 88 - عامل تمایز میلوئید 88TNF-α - فاکتور نکروز توموری آلفاNuclear factor-kappa B - فاکتور هسته ای-کاپا Blipopolysaccharide - لیپوپلی ساکاریدNitrogen monoxide - منوکسید نیتروژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Resolvin D2 recovers neural injury by suppressing inflammatory mediators expression in lipopolysaccharide-induced Parkinson's disease rat model Resolvin D2 recovers neural injury by suppressing inflammatory mediators expression in lipopolysaccharide-induced Parkinson's disease rat model](/preview/png/10752101.png)
چکیده انگلیسی
Activation of microglial cells have been treated as the main role in the pathogenesis of neuropathic inflammation and neurodegenerative disease, including Parkinson's disease (PD), prion disease and Alzheimer's disease (AD). Resolvin D2 (RvD2) is derived from omega-3 polyunsaturated fatty acid and performs potent anti-inflammatory and pro-resolution effects. Here we investigated the effects of intrathecal injection of RvD2 for substantia nigra pars compacta (SNpc) in vivo and primary microglia in vitro experiment on pro-inflammatory cytokine expression and NF-κB activation in Lipopolysaccharide (LPS)-induced PD rat model. The total of 30 days experimental period were used for the rats' experiment, the LPS-induced inflammation in SNpc increase the expression of NO, iNOS, TNF-α, IL-1, IL-18, IL-6, IL-1β, ROS production, the translocation of NF-κB p65, IκBα, and IKKβ expression in glial cells. After injection of RvD2, the treatment prevented development of behavioral defects and TLR4/NF-κB pathway activation. Therefore, we demonstrated a novel role of RvD2 in treatment of rat PD model and LPS activated microglia inflammation. Given the significant potency of RvD2 and well-known side effects of microglia inflammatory inhibitors, it may represent novel hotspot for treating neurodegenerative disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 460, Issue 3, 8 May 2015, Pages 799-805
Journal: Biochemical and Biophysical Research Communications - Volume 460, Issue 3, 8 May 2015, Pages 799-805
نویسندگان
Yuguang Tian, Ying Zhang, Ruoyu Zhang, Song Qiao, Jing Fan,