کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8275233 | 1535105 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Temporal profile of M1 and M2 responses in the hippocampus following early 24Â h of neurotrauma
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کلمات کلیدی
TNFαSiCrRNAqRT-PCRIL-1βFizz-1CCINeurotraumaTBIARG-1IFNγcDNA - cDNAArginase-1 - آرژنین 1Traumatic brain injury - آسیب تروماتیک مغزcomplementary deoxyribonucleic acid - اسید دز اکسید ریبونوکلئیک مکملribosomal ribonucleic acid - اسید ریبونوکلئیک ریبوزومیNeuroinflammation - التهاب عصبیinterferon-gamma - اینترفرون گاماinterleukin-1-β - اینترلوکین-1-βELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاtumor necrosis factor-α - تومور نکروز عامل αquantitative real-time reverse transcription-polymerase chain reaction - زمان واقعی واکنش زنجیره ای رونویسی معکوس و پلیمریزا معکوس کمیPro- and anti-inflammatory cytokines - سیتوکینهای پروتئینی و ضد التهابیcontrolled cortical impact - کنترل قشر مغزی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Traumatic brain injury (TBI) elicits complex inflammatory assets (M1 and M2 responses) in the brain that include the expression of various cytokines/chemokines and the recruitment of blood cells, contributing secondary injury cascades (SIC), and also recovery processes. The modulation of such inflammatory assets might be a therapeutic option following TBI. The present study assesses a temporal profile of various molecular markers of M1 and M2 response in the hippocampus after TBI. Following a unilateral controlled cortical impact (CCI) on young rats, hippocampal tissues of each brain were harvested at 2, 4, 6, 10, and 24 h post trauma. Including shams (craniotomy only), half of the rats were assessed for gene expression and half for the protein of various markers for M1 [interferon-gamma (IFNγ), tumor necrosis factor-α (TNFα), interleukin (IL)-1-β (IL-1β), and IL-6] and M2 [IL-4, IL-10, IL-13, arginase 1 (Arg1), YM1, FIZZ1, and mannose receptor C-1 (MRC1)] responses. Analysis revealed that molecular markers of M1 and M2 responses have heterogeneous injury effects in the hippocampus and that “time-post-injury” is an important factor in determining inflammation status. With the heterogeneous gene expression of pro-inflammatory cytokines, M1 response was significantly elevated at 2 h and declined at 24 h after TBI, however, their levels remained higher than the sham rats. Except IFNγ, proteins of M1 cytokines were significantly elevated in the first 24 h, and peaked between 2-6 h [TNFα (2 h), IL-1β (6 h), and IL-6 (4-6 h)]. With the heterogeneous relative gene expression of Arg1, YM1, FIZZ1, and MRC1, levels of M2 cytokines were peaked at 24 h post TBI. IL-10 and IL-13 expression appeared biphasic in the first 24 h. Protein values of IL-4 and IL-13 peaked at 24 h and IL-10 at 6 h post injury. Results suggest that the M1 response rises rapidly after injury and overpowers the initial, comparatively smaller, or transient M2 response. A treatment that can modulate inflammation, reduce SIC, and improve recovery should be initiated early (within 10 h) after TBI.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of the Neurological Sciences - Volume 357, Issues 1â2, 15 October 2015, Pages 41-49
Journal: Journal of the Neurological Sciences - Volume 357, Issues 1â2, 15 October 2015, Pages 41-49
نویسندگان
Mubeen A. Ansari,