Effect of EPA on inflammatory response of human periodontal ligament fibroblasts induced by P. gingivalis LPS

doi:10.19439/j.sjos.2023.05.005

Abstract

Abstract: PURPOSE: To observe the effect of eicosapentaenoc acid (EPA) on the expression of inflammatory factors in human periodontal ligament fibroblasts (hPDLCs) induced by using lipopolysaccharides (LPS) of Porphyromonas gingivalis (P. gingivalis). METHODS: hPDLCs were cultured by using tissue block method, and the effects of different concentrations of EPA on the activity of hPDLCs cells were observed by MTT method. According to MTT results, the appropriate concentration of EPA was selected, and the expression of interleukin-6(IL-6), IL-8 and IL-1β in hPDLCs induced by P. gingivalis LPS was detected by real time PCR and ELISA. The data were evaluated by SPSS 10.0 software package. RESULTS: 25-100 μmol/L EPA had no effect on the activity of hPDLCs cells, but could inhibit the expression of IL-6, IL-8 and IL-1β induced by P. gingivalis LPS in a dose-dependent manner. CONCLUSIONS: EPA can inhibit the expression of inflammatory factors induced by P. gingivalis LPS without affecting cell activity, indicating that EPA has the possibility of anti-inflammatory treatment of periodontitis.

Key words: Eicosapentaenoic acid, Lipopolysaccharide, Human periodontal ligament fibroblasts, Inflammatory factors

CLC Number:

R781.4

ZHOU Zi-chao, SHU Rong, WU Yi-qun. Effect of EPA on inflammatory response of human periodontal ligament fibroblasts induced by P. gingivalis LPS[J]. Shanghai Journal of Stomatology, 2023, 32(5): 475-479.

References

[1] Heaton B, Dietrich T.Causal theory and the etiology of periodontal diseases[J].Periodontol 2000, 2012, 58(1): 26-36.
[2] Heaton B, Dietrich T.Analytic epidemiology and periodontal diseases[J].Periodontol 2000, 2012, 58(1): 112-120.
[3] Wakabayashi H, Kondo I, Kobayashi T.Periodontitis, periodontopathic bacteria and lactoferrin[J]. Biometals, 2010, 23(3): 419-424.
[4] Liu YC, Lerner UH, Teng YT.Cytokine responses against periodontal infection: protective and destructive roles[J]. Periodontol 2000, 2010, 52(1): 163-206.
[5] Calder PC.Marine omega-3 fatty acids and inflammatory processes: effects, mechanisms and clinical relevance[J]. Biochim Biophys Acta, 2015, 1851(4): 469-484.
[6] Singer P, Shaprio H, Theilla M, et al.Anti-inflammatory properties of omega-3 fatty acids in critical illness: novel mechanisms and an intergrative perspective[J]. Intensive Care Med, 2008, 34(9): 1580-1592.
[7] Rylev M, Kilian M.Prevalence and distribution of principal periodontal pathogens worldwide[J]. J Clin Periodontol, 2008, 35(8 Suppl): 346-361.
[8] How KY, Song KP, Chan KG.Porphyromonas gingivalis: an overview of periodontopathic pathogen below the gum line[J]. Front Microbiol, 2016, 7: 53-67.
[9] Wang XY, Quinn P, et al.Endotoxins: lipopolysaccharides of gram-negative bacteria[J]. Subcell Biochem, 2011, 53: 3-25.
[10] Murray DA, Wilton J.Lipopolysaccharide from the periodontal pathogen Porphyromonas gingivalis prevents apoptosis of HL60-derived neutrophils in vitro[J]. Infect Immun, 2003, 71(12): 7232-7235.
[11] Shaddox LM, Gonçalves PF, Vovk A, et al.LPS-induced inflanimatory response after therapy of aggressive periodontitis[J]. J Dent Res, 2013, 92(8): 702-708.
[12] Holmlund A, Hänström L, Lerner UH.Bone resorbing activity and cytokine levels in gingival crevicular fluid before and after treatment of periodontal disease[J]. J Clin Periodootol, 2004, 31(6): 475-482.
[13] Nakamura I, Jimi E.Regualtion of osteoclast differentiation and function by interleukin-1[J]. Vitam Horm, 2006, 74(1): 357-370.
[14] Tonetti MS, Imboden MA, Gerber I.Localized expression of mRNA for phagocyte-specific chemotactic cytokines in human periodontal infections[J].Infect Immun, 1994, 62(9): 4005-4014.
[15] Xue B, Yang Z, Wang X, et al.Omega-3 polyunsaturated fatty acids antagonize macrophage inflammation via activation of AMPK/SIRT1 pathway[J]. PLoS One, 2012, 7(10): e45990.
[16] Oliver E, McGillicuddy FC, Harford KA, et al. Docosahexaenoic acid attenuates macrophage-induced inflammation and improves insulin sensitivity in adipocytes-specific differential effects between LC n-3 PUFA[J]. J Nutr Biochem, 2012, 23(9): 1192-1200.