search for




 

Anti-Inflammatory Effects of Gelidium amansii Ethanol Extract on Porphyromonas gingivalis Lipopolysacchari-de-Stimulated Human Gingival Fibroblasts through the Regulation of Nuclear Factor Kappa B/Activator Protein-1/Mitogen-Activated Protein Kinase Signaling Pathway
Int J Clin Prev Dent 2018;14(3):197-202
Published online September 30, 2018;  https://doi.org/10.15236/ijcpd.2018.14.3.197
© 2018 International Journal of Clinical Preventive Dentistry.

Chung-Mu Park1, Hyun-Seo Yoon2

Departments of 1Clinical Laboratory Science and 2Dental Hygiene, College of Nursing, Healthcare Sciences and Human Ecology, Dong-Eui University, Busan, Korea
Correspondence to: Hyun-Seo Yoon
Department of Dental Hygiene, College of Nursing and Healthcare Sciences, Dong-Eui University, 176 Eomgwang-ro, Busanjin-gu, Busan 47340, Korea. Tel: +82-51-890-2688, Fax: +82-505-182-6877, E-mail: yoonhs@deu.ac.kr
https://orcid.org/0000-0002-7455-5506
Received June 28, 2018; Revised August 13, 2018; Accepted August 21, 2018.
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.
Abstract
Objective: Gingival inflammation is one of the main causes that can be associated with a lot of periodontal diseases. Among various periodontal pathogens, Porphyromonas gingivalis can be recognized as one of the main causes in the progression of the periodontal inflammation. In this study, the anti-inflammatory activity of Gelidium amansii ethanol extract (GAEE) and its molecular mechanism was investigated in P. gingivalis lipopolysaccharide (LPS-PG) stimulated human gingival fibroblast (HGF)-1 cells.
Methods: The concentration of nitric oxide (NO) and prostaglandin E2 (PGE2) production was estimated by biochemical analysis. Protein expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and their upstream signaling molecules were analyzed by Western blot analysis. 
Results: LPS-PG induced NO and PGE2 production as well as their corresponding enzymes, iNOS and COX-2, were significantly attenuated by GAEE treatment without cytotoxicity. The molecular mechanism was also investigated to determine whether this response was related to the inflammatory transcription factors, nuclear factor (NF)-κB and activator protein (AP)-1, or their upstream signaling molecules, mitogen-activated protein kinases (MAPKs) and phosphoinositide 3-kinase (PI3K)/Akt. Phosphorylated status of p65 and c-jun, each subunit of NF-κB and AP-1, was dose-dependently inhibited by GAEE treatment. In addition, GAEE treatment inhibited phosphorylation of extracellular regulated kinase (ERK) but did not give any effect on other MAPKs and PI3K/Akt signaling molecules.
Conclusion: Consequently, GAEE ameliorates LPS-PG-induced inflammatory responses by blocking NF-κB, AP-1 and ERK activation in HGF-1 cells. Therefore, GAEE may be utilized as a potential anti-inflammatory agent by modulating NO and PGE2 production in the periodontium.
Keywords : Gelidium amansii, inflammation, mitogen-activated protein kinases, NF-kappa B, transcription factor AP-1
References
  1. Lawrence T, Willoughby DA, Gilroy DW. Anti-inflammatory lipid mediators and insights into the resolution of inflammation. Nat Rev Immunol 2002;2:787-95.
    Pubmed CrossRef
  2. How KY, Song KP, Chan KG. Porphyromonas gingivalis: an overview of periodontopathic pathogen below the gum line. Front Microbiol 2016;7:53.
    Pubmed KoreaMed CrossRef
  3. Milward MR, Chapple IL. Classification of periodontal diseases:where were we? Where are we now? Where are we going? Dent Update 2003;30:37-44.
    Pubmed CrossRef
  4. Williams RO, Feldmann M, Maini RN. Anti-tumor necrosis factor ameliorates joint disease in murine collagen-induced arthritis. Proc Natl Acad Sci USA 1992;89:9784-8.
    Pubmed CrossRef
  5. Hajishengallis G, Lamont RJ. Breaking bad: manipulation of the host response by Porphyromonas gingivalis. Eur J Immunol 2014;44:328-38.
    Pubmed KoreaMed CrossRef
  6. Kato H, Taguchi Y, Tominaga K, Umeda M, Tanaka A. Porphyromonas gingivalis LPS inhibits osteoblastic differentiation and promotes pro-inflammatory cytokine production in human periodontal ligament stem cells. Arch Oral Biol 2014;59:167-75.
    Pubmed CrossRef
  7. Sawada N, Ogawa T, Asai Y, Makimura Y, Sugiyama A. Toll-like receptor 4-dependent recognition of structurally different forms of chemically synthesized lipid as of Porphyromonas gingivalis. Clin Exp Immunol 2007;148:529-36.
    Pubmed KoreaMed CrossRef
  8. Li L, Sun W, Wu T, Lu R, Shi B. Caffeic acid phenethyl ester attenuates lipopolysaccharide-stimulated proinflammatory responses in human gingival fibroblasts via NF-κB and PI3K/Akt signaling pathway. Eur J Pharmacol 2017;794:61-8.
    Pubmed CrossRef
  9. Muniz FW, Nogueira SB, Mendes FL, Rösing CK, Moreira MM, de Andrade GM, et al. The impact of antioxidant agents complimentary to periodontal therapy on oxidative stress and periodontal outcomes: a systematic review. Arch Oral Biol 2015;60:1203-14.
    Pubmed CrossRef
  10. Chen YH, Tu CJ, Wu HT. Growth-inhibitory effects of the red alga Gelidium amansii on cultured cells. Biol Pharm Bull 2004;27:180-4.
    Pubmed CrossRef
  11. Yan X, Nagata T, Fan X. Antioxidative activities in some common seaweeds. Plant Foods Hum Nutr 1998;52:253-62.
    Pubmed CrossRef
  12. Fu YW, Hou WY, Yeh ST, Li CH, Chen JC. The immunostimulatory effects of hot-water extract of Gelidium amansii via immersion, injection and dietary administrations on white shrimp Litopenaeus vannamei and its resistance against Vibrio alginolyticus. Fish Shellfish Immunol 2007;22:673-85.
    Pubmed CrossRef
  13. Yuan H, Song J, Li X, Li N, Dai J. Immunomodulation and antitumor activity of kappa-carrageenan oligosaccharides. Cancer Lett 2006;243:228-34.
    Pubmed CrossRef
  14. Kang JH, Lee HA, Kim HJ, Han JS. Gelidium amansii extract ameliorates obesity by down-regulating adipogenic transcription factors in diet-induced obese mice. Nutr Res Pract 2017;11:17-24.
    Pubmed KoreaMed CrossRef
  15. Vodovotz Y, Bogdan C, Paik J, Xie QW, Nathan C. Mechanisms of suppression of macrophage nitric oxide release by transforming growth factor beta. J Exp Med 1993;178:605-13.
    Pubmed CrossRef
  16. Xie WL, Chipman JG, Robertson DL, Erikson RL, Simmons DL. Expression of a mitogen-responsive gene encoding prostaglandin synthase is regulated by mRNA splicing. Proc Natl Acad Sci USA 1991;88:2692-6.
    Pubmed CrossRef
  17. Tabas I, Glass CK. Anti-inflammatory therapy in chronic disease:challenges and opportunities. Science 2013;339:166-72.
    Pubmed KoreaMed CrossRef
  18. Jian CX, Li MZ, Zheng WY, He Y, Ren Y, Wu ZM, et al. Tormentic acid inhibits LPS-induced inflammatory response in human gingival fibroblasts via inhibition of TLR4-mediated NF-kB and MAPK signalling pathway. Arch Oral Biol 2015;60:1327-32.
    Pubmed CrossRef
  19. Kolb H, Kolb-Bachofen V. Nitric oxide: a pathogenetic factor in autoimmunity. Immunol Today 1992;13:157-60.
    CrossRef
  20. Na HK, Surh YJ. Intracellular signaling network as a prime chemopreventive target of (-)-epigallocatechin gallate. Mol Nutr Food Res 2006;50:152-9.
    Pubmed CrossRef
  21. Fujioka S1, Niu J, Schmidt C, Sclabas GM, Peng B, Uwagawa T, et al. NF-kappaB and AP-1 connection: mechanism of NF-kappaB-dependent regulation of AP-1 activity. Mol Cell Biol 2004;24:7806-19.
    Pubmed KoreaMed CrossRef
  22. Mishra S, Tripathi A, Chaudhari BP, Dwivedi PD, Pandey HP, Das M. Deoxynivalenol induced mouse skin cell proliferation and inflammation via MAPK pathway. Toxicol Appl Pharmacol 2014;279:186-97.
    Pubmed CrossRef
  23. Surh YJ. Cancer chemoprevention with dietary phytochemicals. Nat Rev Cancer 2003;3:768-80.
    Pubmed CrossRef


September 2018, 14 (3)