title: Indole-3-carbinol inhibits LPS-induced inflammatory response by blocking TRIF-dependent signaling pathway in macrophages.
abstract: 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.
authors.affiliation: Department of Biotechnology, College of Biomedical and Health Science, Research Institute of Inflammatory Diseases, Konkuk University, Chungju 380-701, Republic of Korea.
authors.forename: Jun
authors.initials: J
authors.lastname: Jiang
authors.forename: Tae Bong
authors.initials: TB
authors.lastname: Kang
authors.forename: Do Wan
authors.initials: do W
authors.lastname: Shim
authors.forename: Na Hyun
authors.initials: NH
authors.lastname: Oh
authors.forename: Tack Joong
authors.initials: TJ
authors.lastname: Kim
authors.forename: Kwang Ho
authors.initials: KH
authors.lastname: Lee
mesh_terms: D033942:Adaptor Proteins, Vesicular Transport / Q000378:metabolism*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002460:Cell Line / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D007211:Indoles / Q000494:pharmacology*; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D011014:Pneumonia / Q000188:drug therapy / Q000209:etiology / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D033942:Adaptor Proteins, Vesicular Transport; D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D007211:Indoles; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D053594:Myeloid Differentiation Factor 88; D009569:Nitric Oxide; C507780:Myd88 protein, mouse; C476286:Ticam1 protein, mouse; C016517:indole-3-carbinol