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      trans-Cinnamaldehyde Reverses Depressive-Like Behaviors in Chronic Unpredictable Mild Stress Rats by Inhibiting NF- κB/NLRP3 Inflammasome Pathway

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          Abstract

          trans-Cinnamaldehyde (TCA) is the main active component extracted from Cinnamomum cassia ( C. cassia), which has many pharmacological effects, such as anti-inflammation, lowering blood glucose, and improving nerve function. However, there is no report of TCA in the treatment of depression. The purpose of this study was to investigate the antidepressant-like effect of TCA and the mechanism of NF kappa B (NF- κB) pathway and NLRP3 inflammasome inhibition by TCA. We divided 40 rats into the control group, CUMS group, FLU group, and the TCA group. The activation of the NF- κB pathway and NLRP3 inflammasome in prefrontal cortex and hippocampus of rats in each group was observed. After the treatments with FLU and TCA, the sucrose consumptions in rats increased significantly and the immobility time in forced swimming was decreased significantly compared to the CUMS group. The expression of TLR4, NF- κB-1, p-p65, TNF- α, NLRP3, ASC, caspase-1, IL-1 β, and IL-18 proteins in prefrontal cortex and hippocampus was decreased, and the expression of IL-1 β, IL-18, and TNF- α in serum was downregulated compared to the CUMS group. Similar to FLU, TCA reverses the depression-like behaviors in rats, which indicates that TCA has a significant antidepressant-like effect. The mechanism of the antidepressant property of TCA might be that it inhibits the activation of the NF- κB pathway and NLRP3 inflammasome in the prefrontal cortex and hippocampus of CUMS rats.

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          The role of inflammation in depression: from evolutionary imperative to modern treatment target.

          Crosstalk between inflammatory pathways and neurocircuits in the brain can lead to behavioural responses, such as avoidance and alarm, that are likely to have provided early humans with an evolutionary advantage in their interactions with pathogens and predators. However, in modern times, such interactions between inflammation and the brain appear to drive the development of depression and may contribute to non-responsiveness to current antidepressant therapies. Recent data have elucidated the mechanisms by which the innate and adaptive immune systems interact with neurotransmitters and neurocircuits to influence the risk for depression. Here, we detail our current understanding of these pathways and discuss the therapeutic potential of targeting the immune system to treat depression.
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            Deubiquitination of NLRP3 by BRCC3 critically regulates inflammasome activity.

            NLRP3 is an important pattern recognition receptor involved in mediating inflammasome activation in response to viral and bacterial infections as well as various proinflammatory stimuli associated with tissue damage or malfunction. Upon activation, NLRP3 assembles a multimeric inflammasome complex comprising the adaptor ASC and the effector pro-caspase-1 to mediate the activation of caspase-1. Although NLRP3 expression is induced by the NF-κB pathway, the posttranscriptional molecular mechanism controlling the activation of NLRP3 remains elusive. Using both pharmacological and molecular approaches, we show that the activation of NLRP3 inflammasome is regulated by a deubiquitination mechanism. We further identify the deubiquitinating enzyme, BRCC3, as a critical regulator of NLRP3 activity by promoting its deubiquitination and characterizing NLRP3 as a substrate for the cytosolic BRCC3-containing BRISC complex. Our results elucidate a regulatory mechanism involving BRCC3-dependent NLRP3 regulation and highlight NLRP3 ubiquitination as a potential therapeutic target for inflammatory diseases. Copyright © 2013 Elsevier Inc. All rights reserved.
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              Inflammation-associated depression: from serotonin to kynurenine.

              In the field of depression, inflammation-associated depression stands up as an exception since its causal factors are obvious and it is easy to mimic in an animal model. In addition, quasi-experimental studies can be carried out in patients who are treated chronically with recombinant cytokines for a medical condition since these patients can be studied longitudinally before, during and after stimulation of the immune system. These clinical studies have revealed that depression is a late phenomenon that develops over a background of early appearing sickness. Incorporation of this feature in animal models of inflammation-associated depression has allowed the demonstration that alterations of brain serotoninergic neurotransmission do not play a major role in the pathogenesis. This is in contrast to the activation of the tryptophan degrading enzyme indoleamine 2,3-dioxygenase that generates potentially neurotoxic kynurenine metabolites such as 3-hydroxy kynurenine and quinolinic acid. Although the relative importance of peripherally versus centrally produced kynurenine and the cellular source of production of this compound remain to be determined, these findings provide new targets for the treatment of inflammation-associated depression that could be extended to other psychiatric conditions mediated by activation of neuroimmune mechanisms. Copyright © 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Evid Based Complement Alternat Med
                Evid Based Complement Alternat Med
                ECAM
                Evidence-based Complementary and Alternative Medicine : eCAM
                Hindawi
                1741-427X
                1741-4288
                2020
                28 February 2020
                28 February 2020
                : 2020
                : 4572185
                Affiliations
                1Chengdu University of TCM, Chengdu 610075, China
                2Shanxi University of Chinese Medicines, Xianyang 712046, China
                Author notes

                Academic Editor: Mark Moss

                Author information
                https://orcid.org/0000-0001-8011-7273
                Article
                10.1155/2020/4572185
                7155764
                32328132
                16ec9565-91e3-44e5-8c52-4791c4dc90d4
                Copyright © 2020 Meng Wang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 19 July 2019
                : 22 September 2019
                : 8 October 2019
                Funding
                Funded by: Science and Technology Coordinated Innovation Project of Shaanxi Province
                Award ID: 2016TTC-S-1-7
                Categories
                Research Article

                Complementary & Alternative medicine
                Complementary & Alternative medicine

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