کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6273428 | 1614803 | 2014 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Aspirin-triggered Lipoxin A4 attenuates mechanical allodynia in association with inhibiting spinal JAK2/STAT3 signaling in neuropathic pain in rats
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کلمات کلیدی
CCILXSALXLXA4cycloxygenase-2Janus Kinase 2ATLSOCSSTAT3JAK2SNLFITCqRT-PCRCOX-2DMSO - DMSOSDS–PAGE - SDS-PAGEchronic constriction injury - آسیب زدگی مزمنSpinal cord injury - آسیب نخاعیsodium dodecyl sulfate–polyacrylamide gel electrophoresis - الکتروفورز ژل دوده سولفات سدیم پلی آکریل آمیدDimethyl sulfoxide - دیمتیل سولفواکسیدsuppressor of cytokine signaling - سرکوب کننده سیگنالینگ سیتوکینCerebral Spinal Fluid - سیالات مغزی نخاعیsci - علمیfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتlipoxygenase - لیپواکسیژنازLipoxins - لیپوکسین هاlipoxin A4 - لیپوکین A4CSF - مایع مغزی نخاعیNaCl solution - محلول NaClquantitative reverse transcription-polymerase chain reaction - واکنش زنجیره ای رونویسی معکوس و پلیمریزا معکوسspinal nerve ligation - پیوند عصب ستون فقراتthreshold cycle - چرخه آستانه
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Aspirin-triggered Lipoxin A4 (ATL), as a Lipoxin A4 (LXA4) epimer, is endogenously produced by aspirin-acetylated cycloxygenase-2 (COX-2) and plays a vital role in endogenous anti-inflammation via the LXA4 receptor (ALX). Recent investigations have indicated that spinal neuroinflammation and the activation of the Janus Kinase 2 (JAK2)/Signal Transducers and Transcription Activators 3 (STAT3) signaling pathway are involved in neuropathic pain states. However, the effect of ATL on neuroinflammation and JAK2/STAT3 signaling in chronic constriction injury (CCI)-induced neuropathic pain in rats has not been well-studied. The present study demonstrated the anti-inflammatory and analgesic effect of ATL on neuropathic pain and assessed the role of spinal JAK2/STAT3 signaling on the effect of ATL. Intrathecal administration of ATL significantly attenuated mechanical allodynia via spinal ALX and inhibited the upregulation of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) on day 7 of CCI surgery. In addition, ATL markedly suppressed the upregulation of p-STAT3 induced by the neuropathic pain. Blockade of JAK2-STAT3 signaling with intrathecal administration of the JAK2 inhibitor AG490 or the STAT3 inhibitor S3I-201 clearly reduced mechanical allodynia and the upregulation of pro-inflammatory cytokines in CCI rats. Interestingly, inhibition of JAK2/STAT3 signaling via ATL or the specific signaling inhibitor (AG49, S3I-201) further promoted the increased expression of suppressor of cytokine signaling 3 (SOCS3) mRNA in the spinal cord induced by CCI surgery. Taken together, our results suggested that the analgesic effect of ATL was mediated by inhibiting spinal JAK2/STAT3 signaling and hence the spinal neuroinflammation in CCI rats.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 273, 25 July 2014, Pages 65-78
Journal: Neuroscience - Volume 273, 25 July 2014, Pages 65-78
نویسندگان
Z.-F. Wang, Q. Li, S.-B. Liu, W.-L. Mi, S. Hu, J. Zhao, Y. Tian, Q.-L. Mao-Ying, J.-W. Jiang, H.-J. Ma, Y.-Q. Wang, G.-C. Wu,