Tea Polyphenols Reducing Lipopolysaccharide-induced Inflammatory Responses in RAW264.7 Macrophages via NF-κB Pathway

Abstract

The anti-inflammatory activity of tea polyphenols(TPs) in RAW264.7 macrophages stimulated by lipopolysaccharide(LPS) was investigated in this paper. RAW264.7 macrophages were treated with different concentrations of TP(0, 12.5, 25, 50, 100, and 200 µg/mL) and then stimulated by LPS. Another blank control group was set up. The expression of pro-inflammatory cytokines associated with the nuclear factor-kappa B(NF-κB) signaling pathway was investigated before and after TP treatment. Pretreatment of RAW264.7 cells with TP decreased the expression of tumor necrosis factor-α(TNF-α), interleukin-6(IL-6) and interleukin 1 beta(IL-1β) pro-inflammatory cytokines. In addition, TP inhibited the phosphorylation of p65 and IκB by blocking the phosphorylation and the degradation of NF-κB inhibitor protein. In conclusion, TP exerts anti-inflammatory effects by regulating the release of inflammatory mediators via the NF-κB signaling pathway.

Keywords

Tea polyphenol / Inflammatory response / RAW264.7 / Nuclear factor-kappa B pathway

References

[1] Cavet M E, Harrington K L, Vollmer T R, Ward K W, Zhang J Z. Mol. Vis., 2011, 17: 533.

[2] Frei B, Higdon J V. J. Nutr., 2003, 133: 3275S.

[3] Takako Y, Takako N, Kitani K. J. Agric. Food Chem., 2002, 50: 3549.

[4] Lagha A B, Grenier D. Sci. Rep., 2016, 6: 34520.

[5] Lambert J D, Sang S, Hong J, Yang C S. J. Agr. Food Chem., 2010, 58: 10016.

[6] Leong D J, Choudhury M, Hanstein R, Hirsh D M, Kim S J, Majeska R J, Schaffler M B, Hardin J A, Spray D C, Goldring M B. Arthritis Res. Ther., 2014, 16: 1.

[7] Relja B, Töttel E, Breig L, Henrich D, Schneider H, Marzi I, Lehnert M. Br. J. Nutr., 2011, 105: 1791.

[8] Sang K H, Sung J, Choi I, Kim Y. Pharmacogn. Mag., 2016, 12: 295.

[9] Benneriah Y, Karin M. Nat. Immunol., 2011, 12: 715.

[10] Lai J L, Liu Y H, Liu C, Qi M P, Liu R N, Zhu X F, Zhou Q G, Chen Y Y, Guo A Z, Hu C M. Inflammation, 2017, 40: 1.

[11] Hayden M S, Ghosh S. Genes Dev., 2012, 26: 203.

[12] Hayden M S, Ghosh S. Cell, 2008, 132: 344.

[13] Lai J. L., Liu Y. H., Peng Y. C., Ge P., He C. F., Liu C., Chen Y. Y., Guo A. Z., Hu C. M., Mediat. Inflamm, 2017, 3082805

[14] Miao J F, Zhu Y M, Gu B B, Wang X B, Zou S X, Deng Y E. Cytokine, 2007, 40: 135.

[15] Watkins L R, Maier S F, Goehler L E. Pain, 1995, 63: 289.

[16] Antwerp D J V, Martin S J, Kafri T, Green D R, Verma I M. Science, 1996, 274: 787.

[17] Lu Y C, Yeh W C, Ohashi P S. Cytokine, 2008, 42: 145.

[18] Chen M, Wang H, Chen W, Meng G. Int. Immunopharmacol., 2011, 11: 549.

[19] Creagh E M, O’Neill L A. Trends Immunol., 2006, 27: 352.

[20] Fitzgerald K A. Eur. J. Immunol., 2010, 40: 595.

[21] Ghosh S, Hayden M S. Immunol. Rev., 2012, 246: 5.

[22] Heine H. Immunol. Lett., 2011, 139: 14.

[23] Ruland J. Nat. Immunol., 2011, 12: 709.

[24] Kim H R, Da Y S, Chung K H. Toxicol. In vitro, 2017, 38: 1.

[25] Kucharczak J, Simmons M J, Fan Y, Gélinas C. Oncogene, 2003, 22: 8961.

[26] Fitzgerald K A, Palsson-Mcdermott E M, Bowie A G, Jefferies C A, Mansell A S, Brady G, Brint E, Dunne A, Gray P, Harte M T. Nature, 2001, 413: 78.

[27] Gurung P, Lukens J R, Kanneganti T. Trends Mol. Med., 2015, 21: 193.

[28] Kawai T, Akira S. Int. Immunol., 2009, 21: 317.

[29] Wree A, Eguchi A, McGeough M D, Pena C A, Johnson C D, Canbay A, Hoffman H M, Feldstein A E. Hepatology, 2014, 59: 898.

[30] Chen S, Sun B. Protein Cell, 2013, 4: 251.

[31] Piette J, Piret B, Bonizzi G, Schoonbroodt S, Merville M P, Legrand-Poels S, Bours V. Biol. Chem., 1997, 378: 1237.