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Updated: Oct 21, 2025
Three-dimensional Inflammatory Human Tissue Equivalents of Gingiva
Published on: April 3, 2018
[Effects of eicosapentaenoic acid on biological activity and inflammatory factor expression of human gingival
Ke-Cong Zhou1, Meng-Jun Sun, Yi-Ru Xia
1Department of Periodontology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology. Shanghai 200011, China.
Purpose:
To explore the effects of eicosapentaenoic acid (EPA) on biological activity and inflammatory factor expression of human gingival fibroblasts (HGFs).
Methods:
The effects of EPA on the activity, morphology and cell cycle of HGFs were observed by living and dead cell staining, immunofluorescence staining and flow cytometry, respectively. HGFs were stimulated by lipopolysaccharides (LPS) of Porphyromonas gingivalis (P. gingivalis) or heat inactivated P. gingivalis, after which the effects of EPA on mRNA and protein expression of IL-6, IL-8 and IL-1β were observed by real-time PCR and ELISA, respectively. The gene and protein expression of heme oxygenase-1(HO-1) was also detected by real-time PCR and Western blotting, respectively. The data were analyzed with SPSS 22.0 software package.
Results:
200 μmol/L EPA inhibited cell activity of HGFs; 100 μmol/L EPA did not affect cell activity and morphology of HGFs, and had no significant effect on cell cycle (P>0.05). EPA significantly downregulated gene expression of IL-6 and IL-1β, and protein expression of IL-6 stimulated by P. gingivalis LPS and heat-killed P.gingivalis(P<0.05), in a dose-dependent manner. EPA increased gene expression of HO-1 in a dose dependent manner(P<0.05), and upregulated HO-1 protein expression.
Conclusions:
EPA significantly inhibits the expression of inflammatory factors without affecting the biological activity of HGFs, which may be related to the induction of HO-1, suggesting the potential role of EPA in the prevention and treatment of periodontitis.
