کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6271473 | 1614762 | 2016 | 17 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Rosuvastatin enhances anti-inflammatory and inhibits pro-inflammatory functions in cultured microglial cells
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کلمات کلیدی
IBA1E18PBSLPSDMEMEAEFBSTBSGAPDHS.D. - SD.experimental autoimmune encephalomyelitis - آنسفالومیلیت خودایمنی تجربیstandard deviation - انحراف معیارinterleukin - اینترلوکینGene expression - بیان ژنAlzheimer’s disease - بیماری آلزایمرTris-buffered saline - تریس بافر شورEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاtumor necrosis factor α - تومور نکروز عامل αEmbryonic day 18 - جنین روز 18cluster of differentiation - خوشه تمایزCNS - دستگاه عصبی مرکزیRoom temperature - دمای اتاقDIV - دیوRosuvastatin - رزوواستاتینdays in vitro - روز in vitrofetal bovine serum - سرم جنین گاوcentral nervous system - سیستم عصبی مرکزیAnti-inflammation - ضد التهابPro-inflammation - طرفدار التهابTNF-α - فاکتور نکروز توموری آلفاPhagocytosis - فاگوسیتوز یا بیگانهخواری lipopolysaccharide - لیپوپلی ساکاریدBacterial lipopolysaccharide - لیپوپلی ساکارید باکتریاییPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریDulbecco’s modified eagle’s medium - محیط عقاب اصلاح شده Dulbeccoionized calcium-binding adaptor molecule 1 - ملکول آداپتور اتصال دهنده کلسیم یونیزه 1Multiple sclerosis - مولتیپل اسکلروزیس(ام اس)
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Rosuvastatin enhances anti-inflammatory and inhibits pro-inflammatory functions in cultured microglial cells Rosuvastatin enhances anti-inflammatory and inhibits pro-inflammatory functions in cultured microglial cells](/preview/png/6271473.png)
چکیده انگلیسی
Microglial activation results in profound morphological, functional and gene expression changes that affect the pro- and anti-inflammatory mechanisms of these cells. Although statins have beneficial effects on inflammation, they have not been thoroughly investigated for their ability to affect microglial functions. Therefore the effects of rosuvastatin, one of the most commonly prescribed drugs in cardiovascular therapy, either alone or in combination with bacterial lipopolysaccharide (LPS), were profiled in pure microglial cultures derived from the forebrains of 18-day-old rat embryos. To reveal the effects of rosuvastatin on a number of pro- and anti-inflammatory mechanisms, we performed morphometric, functional and gene expression studies relating to cell adhesion and proliferation, phagocytosis, pro- and anti-inflammatory cytokine (IL-1β, tumor necrosis factor α (TNF-α) and IL-10, respectively) production, and the expression of various inflammation-related genes, including those related to the above morphological parameters and cellular functions. We found that microglia could be an important therapeutic target of rosuvastatin. In unchallenged (control) microglia, rosuvastatin inhibited proliferation and cell adhesion, but promoted microspike formation and elevated the expression of certain anti-inflammatory genes (Cxcl1, Ccl5, Mbl2), while phagocytosis or pro- and anti-inflammatory cytokine production were unaffected. Moreover, rosuvastatin markedly inhibited microglial activation in LPS-challenged cells by affecting both their morphology and functions as it inhibited LPS-elicited phagocytosis and inhibited pro-inflammatory cytokine (IL-1β, TNF-α) production, concomitantly increasing the level of IL-10, an anti-inflammatory cytokine. Finally, rosuvastatin beneficially and differentially affected the expression of a number of inflammation-related genes in LPS-challenged cells by inhibiting numerous pro-inflammatory and stimulating several anti-inflammatory genes. Since the microglia could elicit pro-inflammatory responses leading to neurodegeneration, it is important to attenuate such mechanisms and promote anti-inflammatory properties, and develop prophylactic therapies. By beneficially regulating both pro- and anti-inflammatory microglial functions, rosuvastatin may be considered as a prophylactic agent in the prevention of inflammation-related neurological disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 314, 9 February 2016, Pages 47-63
Journal: Neuroscience - Volume 314, 9 February 2016, Pages 47-63
نویسندگان
D. Kata, I. Földesi, L.Z. Feher, L. Jr., L.G. Puskas, K. Gulya,