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Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways
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  • 作者:Chang-Bum Ahn ; Won-Kyo Jung ; Sun-Joo Park ; Yong-Tae Kim ; Won-Suk Kim…
  • 关键词:chitosan ; RAW macrophage ; inflammation ; NF ; κB ; AP ; 1 ; MAPK
  • 刊名:Inflammation
  • 出版年:2016
  • 出版时间:February 2016
  • 年:2016
  • 卷:39
  • 期:1
  • 页码:366-374
  • 全文大小:1,479 KB
  • 参考文献:1.Abarikwu, S.O. 2014. Kolaviron, a natural flavonoid from the seeds of Garcinia kola, reduces LPS-induced inflammation in macrophages by combined inhibition of IL-6 secretion, and inflammatory transcription factors, ERK1/2, NF-kappaB, p38, Akt, p-c-JUN and JNK. Biochimica et Biophysica Acta 1840: 2373–81.CrossRef PubMed
    2.Reddy, D.B., and P. Reddanna. 2009. Chebulagic acid (CA) attenuates LPS-induced inflammation by suppressing NF-kappaB and MAPK activation in RAW 264.7 macrophages. Biochemical and Biophysical Research Communication 381: 112–7.CrossRef
    3.Choudhari, A.S., P. Raina, M.M. Deshpande, A.G. Wali, A. Zanwar, S.L. Bodhankar, and R. Kaul-Ghanekar. 2013. Evaluating the anti-inflammatory potential of Tectaria cicutaria L. rhizome extract in vitro as well as in vivo. Journal of Ethnopharmacology 150: 215–22.CrossRef PubMed
    4.Mourya, V.K., and N.N. Inamdar. 2008. Chitosan-modifications and applications: opportunities galore. Reactive and Functional Polymers 68: 1013–51.CrossRef
    5.Cho, Y.S., S.K. Kim, C.B. Ahn, and J.Y. Je. 2011. Preparation, characterization, and antioxidant properties of gallic acid-grafted-chitosans. Carbohydrate Polymers 83: 1617–22.CrossRef
    6.Cho, Y.S., S.K. Kim, and J.Y. Je. 2011. Chitosan gallate as potential antioxidant biomaterial. Bioorganic & Medicinal Chemistry Letters 21: 3070–3.CrossRef
    7.Lee, D.S., S.H. Eom, Y.M. Kim, H.S. Kim, M.J. Yim, S.H. Lee, D.H. Kim, and J.Y. Je. 2014. Antibacterial and synergic effects of gallic acid-grafted-chitosan with beta-lactams against methicillin-resistant Staphylococcus aureus (MRSA). Canadian Journal of Microbiology 60: 629–38.CrossRef PubMed
    8.Lee, D.S., and J.Y. Je. 2013. Gallic acid-grafted-chitosan inhibits foodborne pathogens by a membrane damage mechanism. Journal of Agricultural and Food Chemistry 61: 6574–9.CrossRef PubMed
    9.Green, L.C., D.A. Wagner, J. Glogowski, P.L. Skipper, J.S. Wishnok, and S.R. Tannenbaum. 1982. Analysis of nitrate, nitrite, and [15N] nitrate in biological fluids. Analytical Biochemistry 126: 131–8.CrossRef PubMed
    10.Lai, C.S., Y.S. Lai, D.H. Kuo, C.H. Wu, C.T. Ho, and M.H. Pan. 2011. Magnolol potently suppressed lipopolysaccharide-induced iNOS and COX-2 expression via downregulating MAPK and NF-κB signaling pathway. Journal of Functional Foods 3: 198–206.
    11.Kim, H.K., B.S. Cheon, Y.H. Kim, S.Y. Kim, and H.P. Kim. 1999. Effects of naturally occurring flavonoids on nitric oxide production in the macrophage cell line RAW264.7 and their structure-activity relationships. Biochemical Pharmacology 58: 759–65.CrossRef PubMed
    12.Salvemini, D., T.P. Misko, J.L. Masferrer, K. Seibert, M.G. Currie, and P. Needleman. 1993. Nitric oxide activates cyclooxygenase enzymes. Proceedings of the National Academy of Science of the United States of America 90: 7240–4.CrossRef
    13.Kim, J.-A., B.-N. Ahn, C.-S. Kong, and S.-K. Kim. 2011. Anti-inflammatory action of sulfated glucosamine on cytokine regulation in LPS-activated PMA-differentiated THP-1 macrophages. Inflammation Research 60: 1131–8.CrossRef PubMed
    14.Seyidova, D., A. Aliyev, N. Rzayev, M. Obrenovich, B.T. Lamb, M.A. Smith, J.C. De La Torre, G. Perry, and G. Aliev. 2004. The role of nitric oxide in the pathogenesis of brain lesions during the development of Alzheimer’s disease. In Vivo 18: 325–34.PubMed
    15.Cho, Y.-S., S.-H. Lee, S.-K. Kim, C.-B. Ahn, and J.-Y. Je. 2011. Aminoethyl-chitosan inhibits LPS-induced inflammatory mediators, iNOS and COX-2 expression in RAW264. 7 mouse macrophages. Process Biochemistry 46: 465–70.CrossRef
    16.Chou, T.-C., E. Fu, and E. Shen. 2003. Chitosan inhibits prostaglandin E2 formation and cyclooxygenase-2 induction in lipopolysaccharide-treated RAW 264.7 macrophages. Biochemical and Biophysical Research Communication 308: 403–7.CrossRef
    17.Rajapakse, N., M.M. Kim, E. Mendis, and S.K. Kim. 2008. Inhibition of inducible nitric oxide synthase and cyclooxygenase‐2 in lipopolysaccharide‐stimulated RAW264. 7 cells by carboxybutyrylated glucosamine takes place via down‐regulation of mitogen‐activated protein kinase‐mediated nuclear factor‐κB signaling. Immunology 123: 348–57.PubMedCentral CrossRef PubMed
    18.Yoon, W.J., J.Y. Moon, G. Song, Y.K. Lee, M.S. Han, J.S. Lee, B.S. Ihm, W.J. Lee, N.H. Lee, and C.G. Hyun. 2010. Artemisia fukudo essential oil attenuates LPS-induced inflammation by suppressing NF-kappaB and MAPK activation in RAW 264.7 macrophages. Food and Chemical Toxicology 48: 1222–9.CrossRef PubMed
    19.Heo, S.K., H.S. Yi, H.J. Yun, C.H. Ko, J.W. Choi, and S.D. Park. 2010. Ethylacetate extract from Draconis Resina inhibits LPS-induced inflammatory responses in vascular smooth muscle cells and macrophages via suppression of ROS production. Food and Chemical Toxicology 48: 1129–36.CrossRef PubMed
    20.Kundu, J.K., Y.K. Shin, and Y.-J. Surh. 2006. Resveratrol modulates phorbol ester-induced pro-inflammatory signal transduction pathways in mouse skin in vivo: NF-κB and AP-1 as prime targets. Biochemical Pharmacology 72: 1506–15.CrossRef PubMed
    21.Casettari, L., L. Gennari, D. Angelino, P. Ninfali, and E. Castagnino. 2012. ORAC of chitosan and its derivatives. Food Hydrocolloids 28: 243–7.
    22.Whitmarsh, A., and R. Davis. 1996. Transcription factor AP-1 regulation by mitogen-activated protein kinase signal transduction pathways. Journal of Molecular Medicine 74: 589–607.CrossRef PubMed
    23.Silvers, A.L., M.A. Bachelor, and G.T. Bowden. 2003. The role of JNK and p38 MAPK activities in UVA-induced signaling pathways leading to AP-1 activation and c-Fos expression. Neoplasia (New York, NY) 5: 319.CrossRef
    24.Giri, R.S., H.M. Thaker, T. Giordano, J. Williams, D. Rogers, V. Sudersanam, and K.K. Vasu. 2009. Design, synthesis and characterization of novel 2-(2, 4-disubstituted-thiazole-5-yl)-3-aryl-3H-quinazoline-4-one derivatives as inhibitors of NF-κB and AP-1 mediated transcription activation and as potential anti-inflammatory agents. European Journal of Medicinal Chemistry 44: 2184–9.CrossRef PubMed
    25.Franklin, C.C., and A.S. Kraft. 1997. Conditional expression of the mitogen-activated protein kinase (MAPK) phosphatase MKP-1 preferentially inhibits p38 MAPK and stress-activated protein kinase in U937 cells. Journal of Biological Chemistry 272: 16917–23.CrossRef PubMed
    26.Hazzalin, C.A., and L.C. Mahadevan. 2002. MAPK-regulated transcription: a continuously variable gene switch? Nature Reviews Molecular Cell Biology 3: 30–40.CrossRef PubMed
    27.Kaminska, B. 2005. MAPK signalling pathways as molecular targets for anti-inflammatory therapy from molecular mechanisms to therapeutic benefits. Biochimica et Biophysica Acta 1754: 253–62.CrossRef PubMed
    28.Uto, T., M. Fujii, and D.X. Hou. 2005. 6-(Methylsulfinyl)hexyl isothiocyanate suppresses inducible nitric oxide synthase expression through the inhibition of Janus kinase 2-mediated JNK pathway in lipopolysaccharide-activated murine macrophages. Biochemical Pharmacology 70: 1211–21.CrossRef PubMed
    29.Surh, Y.J., K.S. Chun, H.H. Cha, S.S. Han, Y.S. Keum, K.K. Park, and S.S. Lee. 2001. Molecular mechanisms underlying chemopreventive activities of anti-inflammatory phytochemicals: down-regulation of COX-2 and iNOS through suppression of NF-kappa B activation. Mutation Research 480–481: 243–68.CrossRef PubMed
  • 作者单位:Chang-Bum Ahn (1)
    Won-Kyo Jung (2)
    Sun-Joo Park (3)
    Yong-Tae Kim (4)
    Won-Suk Kim (5)
    Jae-Young Je (6)

    1. Division of Food and Nutrition, Chonnam National University, Gwangju, 550-757, Republic of Korea
    2. Department of Biomedical Engineering, Pukyong National University, Busan, 608-737, Republic of Korea
    3. Department of Chemistry, Pukyong National University, Busan, 608-737, Republic of Korea
    4. Department of Food Science and Biotechnology, Kunsan National University, Kunsan, 573-701, Republic of Korea
    5. Major in Pharmaceutical Engineering, Division of Bioindustry, Silla University, Busan, 46958, Republic of Korea
    6. Department of Marine-Bio Convergence Science, Pukyong National University, Busan, 608-739, Republic of Korea
  • 刊物类别:Medicine
  • 刊物主题:Medicine & Public Health
    Rheumatology
    Internal Medicine
    Pharmacology and Toxicology
    Pathology
  • 出版者:Springer Netherlands
  • ISSN:1573-2576
文摘
Chitosan is a naturally occurring polysaccharide, which has exhibited antioxidant, antimicrobial, and anti-cancer activities among others. Modification of chitosan by grafting phenolic compounds is a good strategy for improvement of bioactivities of chitosan. We investigated the anti-inflammatory action of gallic acid-grafted-chitosan (GAC) in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. GAC inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) by inhibiting inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in LPS-stimulated RAW264.7 macrophages. GAC also suppressed the production and mRNA expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). GAC inactivated nuclear factor-κB (NF-κB) via inhibiting the phosphorylation and degradation of the NF-κB inhibitor, IκB. In addition, GAC suppresses the activation of activator protein-1 (AP-1) through the phosphorylation of mitogen-activated protein kinase (MAPK) such as extracellular signal-regulated kinase (ERK1/2), p38 MAPK, and c-Jun N-terminal kinase/stress-activated protein kinase (JNK). These results suggest that GAC has the potential anti-inflammatory action by downregulating transcriptional factors (NF-κB and AP-1) through MAPK signaling pathways. KEY WORDS chitosan RAW macrophage inflammation NF-κB AP-1 MAPK

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