کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
914520 | 918401 | 2010 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Spinal macrophage migration inhibitory factor contributes to the pathogenesis of inflammatory hyperalgesia in rats
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کلمات کلیدی
N-methyl-d-aspartatep-p38 MAPKJAK-STATCD74NMDARPI3KERKMAPK - MAPKNMDA receptor - NMDA گیرندهTautomerase - تائوتومرازInflammatory pain - درد التهابیextracellular signal regulated kinase - سیگنال خارج سلولی kinase را تنظیم می کندMIF - شهرMacrophage migration inhibitory factor - عامل مهارکننده مهاجرت ماکروفاژCSF - مایع مغزی نخاعیCerebrospinal fluid - مایع مغزی نخاعیJanus kinase-signal transducer and activator of transcription - مبدل سیگنال ژنوس کیناز و فعال کننده رونویسیmitogen-activated protein kinase - پروتئین کیناز فعال با mitogen
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Spinal macrophage migration inhibitory factor contributes to the pathogenesis of inflammatory hyperalgesia in rats Spinal macrophage migration inhibitory factor contributes to the pathogenesis of inflammatory hyperalgesia in rats](/preview/png/914520.png)
چکیده انگلیسی
Pro-inflammatory cytokine production after nociceptive stimuli is pivotal for hyperalgesia. As macrophage migration inhibitory factor (MIF), a pleiotropic cytokine produced mainly by nonneuronal tissue, has been involved in the regulation of neuronal functions, herein we examined the role for MIF in formalin-induced inflammatory pain model. MIF critically contributed to nociceptive behaviors following formalin injection. Specifically, spinal administration of a MIF inhibitor (ISO-1) prevented and reversed flinching responses in rats. Further examination showed that levels of both MIF and the MIF receptor CD74 were substantially increased within the ipsilateral spinal cord dorsal horn after formalin administration. Mechanistic studies revealed that MIF upregulated the expression of the spinal NMDA receptor subunit NR2B via the MAPK signaling pathway. Moreover, microglial cells were found to be the major source of spinal MIF after formalin administration by fluorescence colocalization. These data highlight spinal MIF plays a critical role in the pathogenesis of formalin-induced inflammatory pain and suggest MIF may be a potential target for therapy of such pathological condition.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: PAIN - Volume 148, Issue 2, February 2010, Pages 275-283
Journal: PAIN - Volume 148, Issue 2, February 2010, Pages 275-283
نویسندگان
FuZhou Wang, XiaoFeng Shen, XiRong Guo, YuZhu Peng, YuSheng Liu, ShiQin Xu, Jie Yang,