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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
© 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:
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 ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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

September 2018, 14 (3)