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      Increased cerebral nuclear factor kappa B in a complex regional pain syndrome rat model: possible relationship between peripheral injury and the brain

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          Abstract

          Purpose

          Complex regional pain syndrome (CRPS) is a rare but refractory pain disorder. Recent advanced information retrieval studies using text-mining and network analysis have suggested nuclear factor kappa B (NFκB) as a possible central mediator of CRPS. The brain is also known to play important roles in CRPS. The aim of this study was to evaluate changes in cerebral NFκB in rats with CRPS.

          Materials and methods

          The chronic post-ischemia perfusion (CPIP) model was used as the CRPS animal model. O-rings were applied to the left hind paws of the rats. The rats were categorized into three groups according to the results of behavioral tests: the CPIP-positive (A) group, the CPIP-negative (B) group, and the control (C) group. Three weeks after the CPIP procedure, the right cerebrums of the animals were harvested to measure NFκB levels using an ELISA.

          Results

          Animals in group A had significantly decreased mechanical pain thresholds ( P<0.01) and significantly increased cerebral NFκB when compared to those in groups B and C ( P=0.024).

          Conclusion

          This finding indicates that peripheral injury increases cerebral NFκB levels and implies that minor peripheral injury can lead to the activation of pain-related cerebral processes in CRPS.

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          Most cited references 47

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          Quantitative assessment of tactile allodynia in the rat paw.

           J Pogrel,  F. Bach,  T L Yaksh (1994)
          We applied and validated a quantitative allodynia assessment technique, using a recently developed rat surgical neuropathy model wherein nocifensive behaviors are evoked by light touch to the paw. Employing von Frey hairs from 0.41 to 15.1 g, we first characterized the percent response at each stimulus intensity. A smooth log-linear relationship was observed, with a median 50% threshold at 1.97 g (95% confidence limits, 1.12-3.57 g). Subsequently, we applied a paradigm using stimulus oscillation around the response threshold, which allowed more rapid, efficient measurements. Median 50% threshold by this up-down method was 2.4 g (1.81-2.76). Correlation coefficient between the two methods was 0.91. In neuropathic rats, good intra- and inter-observer reproducibility was found for the up-down paradigm; some variability was seen in normal rats, attributable to extensive testing. Thresholds in a sizable group of neuropathic rats showed insignificant variability over 20 days. After 50 days, 61% still met strict neuropathy criteria, using survival analysis. Threshold measurement using the up-down paradigm, in combination with the neuropathic pain model, represents a powerful tool for analyzing the effects of manipulations of the neuropathic pain state.
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            Introduction to NF-kappaB: players, pathways, perspectives.

             Ian Gilmore (2006)
            This article serves as an introduction to the collection of reviews on nuclear factor-kappaB (NF-kappaB). It provides an overview of the discovery and current status of NF-kappaB as a research topic. Described are the structures, activities and regulation of the proteins in the NF-kappaB family of transcription factors. NF-kappaB signaling is primarily regulated by inhibitor kappaB (IkappaB) proteins and the IkappaB kinase complex through two major pathways: the canonical and non-canonical NF-kappaB pathways. The organization and focus of articles included in the following reviews are described, as well as likely future areas of research interest on NF-kappaB.
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              NF-kappaB and the immune response.

              One of the primary physiological roles of nuclear factor-kappa B (NF-kappaB) is in the immune system. In particular, NF-kappaB family members control the transcription of cytokines and antimicrobial effectors as well as genes that regulate cellular differentiation, survival and proliferation, thereby regulating various aspects of innate and adaptive immune responses. In addition, NF-kappaB also contributes to the development and survival of the cells and tissues that carry out immune responses in mammals. This review, therefore, describes the role of the NF-kappaB pathway in the development and functioning of the immune system.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2019
                06 March 2019
                : 12
                : 909-914
                Affiliations
                [1 ]Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Seongnam, South Korea, painfree@ 123456snubh.org
                [2 ]College of Medicine, Seoul National University, Seoul, South Korea, painfree@ 123456snubh.org
                [3 ]Laboratory of Veterinary Anatomy, College of Veterinary Medicine, Konkuk University, Seoul, South Korea
                [4 ]Department of Anesthesiology and Pain Medicine, Ajou University Hospital, Suwon, South Korea
                Author notes
                Correspondence:, Pyung Bok Lee, Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Gumi-dong 300, Bundang-gu, Seongnam-si, 13620, South Korea, Tel +82 31 787 7499, Fax +82 31 787 4063, Email painfree@ 123456snubh.org
                jpr-12-909
                10.2147/JPR.S166270
                6408925
                © 2019 Nahm et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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