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Zwolinska-Wcislo M, Krzysiek-Maczka G, Ptak-Belowska A, Karczewska E, Pajdo R, Sliwowski Z, et al. Antibiotic treatment with ampicillin accelerates the healing of colonic damage impaired by aspirin and coxib in the experimental colitis. Importance of intestinal bacteria, colonic microcirculation and proinflammatory cytokines. J Physiol Pharmacol. 2011; 62(3): 357-68.

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Article

Silibinin Suppresses Mediators of Inflammation through the Inhibition of TLR4-TAK1 Pathway in LPS-induced RAW264.7 Cells

1Department of Food Science and Biotechnology, CHA University, Kyonggi 463-400, South Korea


Journal of Food and Nutrition Research. 2016, Vol. 4 No. 8, 515-521
DOI: 10.12691/jfnr-4-8-5
Copyright © 2016 Science and Education Publishing

Cite this paper:
Ji-Hyeon Song, Kui-Jin Kim, Boo-Yong Lee. Silibinin Suppresses Mediators of Inflammation through the Inhibition of TLR4-TAK1 Pathway in LPS-induced RAW264.7 Cells. Journal of Food and Nutrition Research. 2016; 4(8):515-521. doi: 10.12691/jfnr-4-8-5.

Correspondence to: Boo-Yong  Lee, Department of Food Science and Biotechnology, CHA University, Kyonggi 463-400, South Korea. Email: bylee@cha.ac.kr

Abstract

Silibinin is the major bioactive compound of silymarin which is the mixture of flavonolignans extracted from milk thistle. Silibinin has been shown to possess anti-inflammatory activity. However, the underlying mechanisms still remain unclear. The aims of this study were to determine the effect of silibinin on molecular mechanism in lipopolysaccharide (LPS)-induced RAW264.7 macrophage cells. Here, we observed that silibinin attenuated the production of nitric oxide (NO) and its regulatory protein inducible nitric oxide synthase (iNOS) expression. The pro-inflammatory cytokine interleukin (IL)-1β was inhibited by silibinin in a time dependent manner. Moreover, silibinin decreased the expression of toll-like receptor (TLR)-4, TAK1, and IRF3. TLR- associated MAPK signaling pathway was also dramatically down-regulated in LPS-induced RAW 264.7 cells with presence of silibinin. Silibinin repressed oxidative stress-associated proteins including NOX4, G6PDH, and CuZnSOD, while silibinin increased the expression of GR and catalase in LPS-induced RAW264.7 cells. In the current study, silibinin suppresses the LPS-induced inflammation via modulation of TLR4-TAK1 signaling and subsequently attenuated the production of inflammation mediators in RAW264.7 cells. Therefore, we suggest that silibinin has a potential bioactivity for prevention and intervention of endotoxin-mediated inflammation and TLR4-TAK1-associated chronic diseases.

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