کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8337608 | 1540677 | 2013 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties
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کلمات کلیدی
LPSRegulated on activation normal T cell expressed and secretedM-CSFAβEGCGGAPDHCOX-2ICAM-1intracerebroventriculariNOSICVMCP-1APP(−)-Epigallocatechin-3-gallate - (-) - Epigallocatechin-3-gallateamyloid-beta - آمیلوئید بتاinterleukin - اینترلوکینAlzheimer's disease - بیماری آلزایمرtumor necrosis factor-α - تومور نکروز عامل αintraperitoneal - داخل صفاقیinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییCyclooxygenase-2 - سیکلوکوکسیژناز2TNF-α - فاکتور نکروز توموری آلفاlipopolysaccharide - لیپوپلی ساکاریدmacrophage colony-stimulating factor - ماکروفاژ عامل کلونی تحریک کنندهRANTES - مطالبintercellular adhesion molecule-1 - مولکول چسبندگی بین سلولی -1Monocyte chemotactic protein-1 - پروتئین chemotactic monocyte-1β-amyloid precursor protein - پروتئین پیش ماده β-آمیلوئیدamyloid peptide - پپتید آمیلوئیدGreen tea - چای سبزglyceraldehydes-3-phosphate dehydrogenase - گلیسرالید هیدروژن 3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Neuroinflammation has been known to play a critical role in the pathogenesis of Alzheimer's disease (AD) through amyloidogenesis. In a previous study, we found that systemic inflammation by intraperitoneal (ip) injection of lipopolysaccharide (LPS) induces neuroinflammation and triggers memory impairment. In this present study, we investigated the inhibitory effects of epigallocatechin-3-gallate (EGCG) on the systemic inflammation-induced neuroinflammation and amyloidogenesis as well as memory impairment. ICR mice were orally administered with EGCG (1.5 and 3 mg/kg) for 3 weeks, and then the mice were treated by ip injection of LPS (250 μg/kg) for 7 days. We found that treatment of LPS induced memory-deficiency-like behavior and that EGCG treatment prevented LPS-induced memory impairment and apoptotic neuronal cell death. EGCG also suppressed LPS-induced increase of the amyloid beta-peptide level and the expression of the amyloid precursor protein (APP), β-site APP cleaving enzyme 1 and its product C99. In addition, we found that EGCG prevented LPS-induced activation of astrocytes and elevation of cytokines including tumor necrosis factor-α, interleukin (IL)-1β, macrophage colony-stimulating factor, soluble intercellular adhesion molecule-1 and IL-16, and the increase of inflammatory proteins, such as inducible nitric oxide synthase and cyclooxygenase-2, which are known factors responsible for not only activation of astrocytes but also amyloidogenesis. In the cultured astrocytes, EGCG also inhibited LPS-induced cytokine release and amyloidogenesis. Thus, this study shows that EGCG prevents memory impairment as well as amyloidogenesis via inhibition of neuroinflammatory-related cytokines released from astrocytes and suggests that EGCG might be a useful intervention for neuroinflammation-associated AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Nutritional Biochemistry - Volume 24, Issue 1, January 2013, Pages 298-310
Journal: The Journal of Nutritional Biochemistry - Volume 24, Issue 1, January 2013, Pages 298-310
نویسندگان
Young-Jung Lee, Dong-Young Choi, Yeo-Pyo Yun, Sang Bae Han, Ki-Wan Oh, Jin Tae Hong,