کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11013173 | 1797176 | 2018 | 48 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Curcumin Protects Against Chronic Stress-induced Dysregulation of Neuroplasticity and Depression-like Behaviors via Suppressing IL-1β Pathway in Rats
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کلمات کلیدی
SlingshotPDTCCUMSMPFCADFMDDSSHIL-1βMajor depressive disorder - اختلال افسردگی عمدهDepression - افسردگیNeuroinflammation - التهاب عصبیEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاchronic unpredictable mild stress - تنش خفیف غیر قابل پیش بینی مزمنCin - جینCNS - دستگاه عصبی مرکزیcentral nervous system - سیستم عصبی مرکزیactin-depolymerizing factor - عامل تخلیه کننده اکتینtumor necrosis factor-a - عامل نکروز تومور- aTNF-α - فاکتور نکروز توموری آلفاmedial prefrontal cortex - قشر غده پروسترولNeuroplasticity - نوروپلاستیpyrrolidinedithiocarbamate - پیرولیدیدیتیو کرباماتCurcumin - کورکومینCofilin - کوفیلین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Accumulating evidence has accrued demonstrating that inflammatory processes in the central nervous system (CNS) are associated with various neurological disorders including depression. However, whether inflammation-mediated neuronal damage is involved in depression-like behaviors induced by chronic stress and, in particular, whether suppression of inflammation could then serve as a potential strategy in depression therapy remains largely unknown. The present study aimed to investigate the neuronal mechanisms and signaling pathways through which inflammation results in neuronal deterioration in a rat model of depression and thus identify agents with potential roles as antidepressant treatments. Our results showed that chronic unpredictable mild stress (CUMS) exposure induced microglia activation and overexpression of the cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-a (TNF-α) within the medial prefrontal cortex (mPFC), effects which were paralleled with neuronal structural changes. In contrast, chronic administration of either IL-1β or nuclear factor κB (NF-κB) antagonists significantly ameliorated this dysregulation of neuronal structure and biochemical parameters such as SSH1 and phospho-cofilin within the mPFC, as well as the display of depression-like behaviors induced by CUMS exposure. More importantly, pretreatment with curcumin (40â¯mg/kg, i.p., 5â¯weeks), produced antidepressant-like actions and repressed the inflammatory responses and neuronal structural abnormalities. These findings reveal some of the molecular neuroinflammation pathways associated with depression and suggest new avenues of investigation for the development of potential antidepressant therapies in the treatment of inflammation-related neuronal deterioration in this disorder.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 392, 10 November 2018, Pages 92-106
Journal: Neuroscience - Volume 392, 10 November 2018, Pages 92-106
نویسندگان
Cuiqin Fan, Qiqi Song, Peng Wang, Ye Li, Mu Yang, Boce Liu, Shu Yan Yu,