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Food Chem Toxicol. 2013 Jul;57:256-61. doi: 10.1016/j.fct.2013.03.040. Epub 2013 Apr 15.

Indole-3-carbinol inhibits LPS-induced inflammatory response by blocking TRIF-dependent signaling pathway in macrophages.

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Department of Biotechnology, College of Biomedical and Health Science, Research Institute of Inflammatory Diseases, Konkuk University, Chungju 380-701, Republic of Korea.


Indole-3-carbinol (I3C), a natural hydrolysis product of glucobrassicin, is a member of the Brassica family of vegetables and is known to have various anti-cancer activities. In the present study, we assessed in vitro and in vivo anti-inflammatory effects of I3C and its molecular mechanisms. I3C attenuated the production of pro-inflammatory mediators such as NO, IL-6, and IL-1β in LPS-induced Raw264.7 cells and THP-1 cells through attenuation of the TRIF-dependent signaling pathway. Furthermore, I3C suppressed the infiltration of immune cells into the lung and pro-inflammatory cytokine production such as IL-6, TNF-α in broncho-alveolar lavage fluid (BALF) in the LPS-induced acute lung injury mouse model. I3C also suppressed IL-1β secretion in nigericin treated in vivo model. I3C has potent anti-inflammatory effects through regulating TRIF-dependent signaling pathways, suggesting that I3C may provide a valuable therapeutic strategy in treating various inflammatory diseases.

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