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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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          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.


          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).


          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 38

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          Roles for NF-kappaB in nerve cell survival, plasticity, and disease.

          Here we review evidence of roles for NF-kappaB in the regulation of developmental and synaptic plasticity, and cell survival in physiological and pathological settings. Signaling pathways modulating NF-kappaB activity include those engaged by neurotrophic factors, neurotransmitters, electrical activity, cytokines, and oxidative stress. Emerging findings support a pivotal role for NF-kappaB as a mediator of transcription-dependent enduring changes in the structure and function of neuronal circuits. Distinct subunits of NF-kappaB may uniquely affect cognition and behavior by regulating specific target genes. NF-kappaB activation can prevent the death of neurons by inducing the production of antiapoptotic proteins such as Bcl-2, IAPs and manganese superoxide dismutase (Mn-SOD). Recent findings indicate that NF-kappaB plays important roles in disorders such as epilepsy, stroke, Alzheimer's and Parkinson's diseases, as well as oncogenesis. Molecular pathways upstream and downstream of NF-kappaB in neurons are being elucidated and may provide novel targets for therapeutic intervention in various neurological disorders.
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            Aberrant nuclear factor-kappaB/Rel expression and the pathogenesis of breast cancer.

            Expression of nuclear factor-kappaB (NF-kappaB)/Rel transcription factors has recently been found to promote cell survival, inhibiting the induction of apoptosis. In most cells other than B lymphocytes, NF-kappaB/Rel is inactive, sequestered in the cytoplasm. For example, nuclear extracts from two human untransformed breast epithelial cell lines expressed only very low levels of NF-kappaB. Unexpectedly, nuclear extracts from two human breast tumor cell lines displayed significant levels of NF-kappaB/Rel. Direct inhibition of this NF-kappaB/ Rel activity in breast cancer cells induced apoptosis. High levels of NF-kappaB/Rel binding were also observed in carcinogen-induced primary rat mammary tumors, whereas only expectedly low levels were seen in normal rat mammary glands. Furthermore, multiple human breast cancer specimens contained significant levels of nuclear NF-kappaB/Rel subunits. Thus, aberrant nuclear expression of NF-kappaB/Rel is associated with breast cancer. Given the role of NF-kappaB/Rel factors in cell survival, this aberrant activity may play a role in tumor progression, and represents a possible therapeutic target in the treatment of these tumors.
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              New insights into the role of nuclear factor-kappaB, a ubiquitous transcription factor in the initiation of diseases.

              Nuclear factor-kappaB (NF-kappaB) is a ubiquitous transcription factor that governs the expression of genes encoding cytokines, chemokines, growth factors, cell adhesion molecules, and some acute phase proteins in health and in various disease states. NF-kappaB is activated by several agents, including cytokines, oxidant free radicals, inhaled particles, ultraviolet irradiation, and bacterial or viral products. Inappropriate activation of NF-kappaB has been linked to inflammatory events associated with autoimmune arthritis, asthma, septic shock, lung fibrosis, glomerulonephritis, atherosclerosis, and AIDS. In contrast, complete and persistent inhibition of NF-kappaB has been linked directly to apoptosis, inappropriate immune cell development, and delayed cell growth. Therefore, development of modulatory strategies targeting this transcription factor may provide a novel therapeutic tool for the treatment or prevention of various diseases.

                Author and article information

                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                06 March 2019
                : 12
                : 909-914
                [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
                © 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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