Effect of Oral Administration of 3,3′-Diindolylmethane on Dextran Sodium Sulfate-Induced Acute Colitis in Mice

• Published in: Journal of agricultural and food chemistry Vol. 64; no. 41; pp. 7702 - 7709
• Main Authors: Jeon, Eun-Joo, Davaatseren, Munkhtugs, Hwang, Jin-Taek, Park, Jae Ho, Hur, Haeng Jeon, Lee, Ae Sin, Sung, Mi Jeong
• Format: Journal Article
• Language: English
• Published: United States American Chemical Society 19.10.2016
• Subjects: lymphangiogenesis; dextran sodium sulfate; 3,3′-diindolylmethane; angiogenesis; inflammatory bowel disease
• ISSN: 0021-8561; 1520-5118
• DOI: 10.1021/acs.jafc.6b02604

In patients with inflammatory bowel disease (IBD), inflammation is induced and maintained by lymphangiogenesis and angiogenesis. 3,3′-Diindolylmethane (DIM) is a natural product formed in acidic conditions from indole-3-carbinol in cruciferous vegetables, and it is known for its chemotherapeutic activity. This study evaluated DIM’s effects on angiogenesis, lymphangiogenesis, and inflammation in a mouse colitis model. Experimental colitis was induced in mice by administering 3% dextran sulfate sodium (DSS) via drinking water. DIM remarkably attenuated the clinical signs and histological characteristics in mice with DSS-induced colitis. DIM suppressed neutrophil infiltration and pro-inflammatory cytokines. Moreover, it significantly suppressed the expression of vascular endothelial growth factor (VEGF)-A and VEGF receptor (VEGFR)-2, indicating that the mechanism may be related to the repression of pro-angiogenesis activity. DIM also remarkably suppressed the expression of VEGF-C, VEGF-D, VEGFR-3, and angiopoietin-2; thus, the mechanism may also be related to the suppression of lymphangiogenesis. Therefore, DIM is a possible treatment option for inflammation of the intestine and associated angiogenesis and lymphangiogenesis