کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
914319 | 1473240 | 2009 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Thrombin receptor: An endogenous inhibitor of inflammatory pain, activating opioid pathways
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کلمات کلیدی
HprtProenkephalinFBSM-CSFDRGGM-CSFPAR1pDynPBSPOMCHBSSBSA - BSAbovine serum albumin - آلبومین سرم گاوinflammation - التهاب( توروم) enkephalin - انکافالینOpioids - اپیوئیدAnalgesia - بیهوشیPain - دردfetal bovine serum - سرم جنین گاوDendritic cell - سلول دندریتیکgranulocyte–macrophage colony-stimulating factor - عامل گرانولوسیت-ماکروفاژ colony-stimulating factormacrophage colony-stimulating factor - ماکروفاژ عامل کلونی تحریک کنندهPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریHanks’ balanced salt solution - محلول نمک متعادل هانکسhypoxanthine phosphoribosyl transferase - هیپوکسانتین فسفریبوسیل ترانسفرازproopiomelanocortin - پروپیوملانوکورتینprodynorphin - پروین دینورفینPENK - پینکdorsal root ganglia - گانگلیس ریشه پشتیprotease-activated receptors - گیرنده فعال فعال پروتئازProtease-activated receptor 1 - گیرنده پروتئاز فعال شده 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Serine proteases such as thrombin, trypsin and mast cell tryptase can act on different cell types through protease-activated receptors (PARs). These receptors have been shown to be implicated in several phenomena such as inflammation, platelet activation, immune response and atherosclerosis. Several studies recently reported PARs expression on neurons and some of them demonstrated that these receptors could interfere with nociception. The contribution of PAR1 to inflammatory pain and the mechanism involved in this phenomenon were investigated. Intraplantar injection of PAR1 agonist increased withdrawal latency and reduced response frequency to von Frey filaments, thus inhibiting nociceptive response to both mechanical and thermal stimuli in mice. PAR1 agonist also reduced carrageenan-induced inflammatory hyperalgesia. The anti-nociceptive effects of PAR1 agonist were mediated by endogenous opioids, as this effect was inhibited by local injection of naloxone methiodide, and because intraplantar injection of PAR1 agonist increased mRNA expression of the endogenous opioid precursor proenkephalin. However, PAR1 agonist was not able to inhibit calcium signals in isolated sensory neurons exposed to pro-nociceptive agents. Finally, despite similar inflammatory parameters, PAR1-deficient mice showed a strong potentiation of inflammatory hyperalgesia induced by the intraplantar injection of either formalin or carrageenan, or in the chronic model of collagen-induced arthritis, compared to wild-type mice. This study highlights a previously unknown endogenous mechanism of analgesia, showing a central role for the thrombin receptor PAR1 in the regulation of inflammatory pain and as an activator of opioid pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: PAIN - Volume 146, Issues 1â2, November 2009, Pages 121-129
Journal: PAIN - Volume 146, Issues 1â2, November 2009, Pages 121-129
نویسندگان
Laurence Martin, Céline Augé, Jérôme Boué, Michelle C. Buresi, Kevin Chapman, Samuel Asfaha, Patricia Andrade-Gordon, Martin Steinhoff, Nicolas Cenac, Gilles Dietrich, Nathalie Vergnolle,