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      Floridoside suppresses pro-inflammatory responses by blocking MAPK signaling in activated microglia

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          Abstract

          Inflammatory conditions mediated by activated microglia lead to chronic neuro-degenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. This study was conducted to determine the effect of floridoside isolated from marine red algae Laurencia undulata on LPS (100 ng/ml) activated inflammatory responses in BV-2 microglia cells. The results show that floridoside has the ability to suppress pro-inflammatory responses in microglia by markedly inhibiting the production of nitric oxide (NO) and reactive oxygen species (ROS). Moreover, floridoside down-regulated the protein and gene expression levels of iNOS and COX-2 by significantly blocking the phosphorylation of p38 and ERK in BV-2 cells. Collectively, these results indicate that floridoside has the potential to be developed as an active agent for the treatment of neuro-inflammation. [BMB Reports 2013; 46(8): 398-403]

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          Activation of innate immunity in the CNS triggers neurodegeneration through a Toll-like receptor 4-dependent pathway.

          Seija Lehnardt, Leon Massillon, Pamela Follett … (2003)
          Innate immunity is an evolutionarily ancient system that provides organisms with immediately available defense mechanisms through recognition of pathogen-associated molecular patterns. We show that in the CNS, specific activation of innate immunity through a Toll-like receptor 4 (TLR4)-dependent pathway leads to neurodegeneration. We identify microglia as the major lipopolysaccharide (LPS)-responsive cell in the CNS. TLR4 activation leads to extensive neuronal death in vitro that depends on the presence of microglia. LPS leads to dramatic neuronal loss in cultures prepared from wild-type mice but does not induce neuronal injury in CNS cultures derived from tlr4 mutant mice. In an in vivo model of neurodegeneration, stimulating the innate immune response with LPS converts a subthreshold hypoxic-ischemic insult from no discernable neuronal injury to severe axonal and neuronal loss. In contrast, animals bearing a loss-of-function mutation in the tlr4 gene are resistant to neuronal injury in the same model. The present study demonstrates a mechanistic link among innate immunity, TLRs, and neurodegeneration.
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            Inflammatory neurodegeneration and mechanisms of microglial killing of neurons.

            Guy Brown, Jonas J. Neher (2010)
            Inflammatory neurodegeneration contributes to a wide variety of brain pathologies. A number of mechanisms by which inflammatory-activated microglia and astrocytes kill neurons have been identified in culture. These include: (1) acute activation of the phagocyte NADPH oxidase (PHOX) found in microglia, (2) expression of the inducible nitric oxide synthase (iNOS) in glia, and (3) microglial phagocytosis of neurons. Activation of PHOX (by cytokines, beta-amyloid, prion protein, lipopolysaccharide, ATP, or arachidonate) causes microglial proliferation and inflammatory activation; thus, PHOX is a key regulator of inflammation. However, activation of PHOX alone causes little or no death, but when combined with iNOS expression results in apparent apoptosis via peroxynitrite production. Nitric oxide (NO) from iNOS expression also strongly synergizes with hypoxia to induce neuronal death because NO inhibits cytochrome oxidase in competition with oxygen, resulting in glutamate release and excitotoxicity. Finally, microglial phagocytosis of these stressed neurons may contribute to their loss.
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              Inducible isoforms of cyclooxygenase and nitric-oxide synthase in inflammation.

              Laurie A. Tomlinson, J R Vane, J Croxtall … (1994)
              Cyclooxygenase (COX) converts arachidonic acid to prostaglandin H2, which is further metabolized to prostanoids. Two isoforms of COX exist: a constitutive (COX-1) and an inducible (COX-2) enzyme. Nitric oxide is derived from L-arginine by isoforms of nitric-oxide synthase (NOS; EC 1.14.13.39): constitutive (cNOS; calcium-dependent) and inducible (iNOS; calcium-independent). Here we have investigated inducible isoforms of COX and NOS in the acute, chronic, and resolving stages of a murine air pouch model of granulomatous inflammation. COX and NOS activities were measured in skin samples in the acute phase, up to 24 h. Activities in granulomatous tissue were measured at 3, 5, 7, 14, and 21 days for the chronic and resolving stages of inflammation. COX-1 and COX-2 proteins were assessed by Western blot. COX activity in the skin increased over the first 24 h and continued to rise up to day 14. COX-2 protein rose progressively, also peaking at day 14. COX-1 protein remained unaltered throughout. The iNOS activity increased over the first 24 h in the skin, with a further major increase in the granulomatous tissue between days 3 and 7, followed by a decrease at day 14 and a further increase at day 21. The rise in COX and NOS activities in the skin during the acute phase reinforces the proinflammatory role for prostanoids and suggests one also for nitric oxide. However, in the chronic and resolving stages, a dissociation of COX and NOS activity occurred. Thus, there may be differential regulation of these enzymes, perhaps due to the changing pattern of cytokines during the inflammatory response.
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                Author and article information

                Journal
                Journal ID (nlm-ta): BMB Rep
                Journal ID (iso-abbrev): BMB Rep
                Journal ID (publisher-id): ksbmb
                Title: BMB reports
                Publisher: Korean Society for Biochemistry and Molecular Biology
                ISSN (Print): 1976-6696
                ISSN (Electronic): 1976-670X
                Publication date (Print): August 2013
                Volume: 46
                Issue: 8
                Pages: 398-403
                Affiliations
                [1 ]Department of Chemistry, Pukyong National University, Busan 608-737, Korea
                [2 ]School of Pharmacy, The University of Queensland, Brisbane, Qld 4072, Australia
                [3 ]Marine Bioprocess Research Center, Pukyong National University, Busan 608-737, Korea
                Author notes
                [* ]Corresponding author. Tel: +82-51-629-7094; Fax: +82-51-629-7099; E-mail: sknkim@ 123456pknu.ac.kr
                Article
                Publisher ID: BMB-46-398
                DOI: 10.5483/BMBRep.2013.46.8.237
                PMC ID: 4133907
                PubMed ID: 23977987
                SO-VID: f09e7e01-70f0-45f5-991d-f59a7449bf2e
                Copyright © Copyright © 2013, Korean Society for Biochemistry and Molecular Biology
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 19 November 2012
                Date revision received : 13 December 2012
                Date accepted : 27 January 2013
                Categories
                Subject: Articles

                Keywords: alzheimer’s disease,floridoside,laurencia undulata,neuro-inflammation,oxidative stress
                Data availability:
                Keywords: alzheimer’s disease, floridoside, laurencia undulata, neuro-inflammation, oxidative stress

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