3,3'-Diindolylmethane inhibits lipopolysaccharide-induced microglial hyperactivation and attenuates brain inflammation

Toxicol Sci. 2014 Jan;137(1):158-67. doi: 10.1093/toxsci/kft240. Epub 2013 Oct 26.

Abstract

Recent studies have revealed that microglial hyperactivation and neuroinflammation are implicated in development and progression of neurodegenerative diseases. In this study, we examined the beneficial effects of 3,3'-diindolylmethane (DIM) and indole-3-carbinol (I3C), dietary components found in cruciferous vegetables, on brain inflammation. DIM, a major metabolite of I3C, suppressed lipopolysaccharide (LPS)-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 in BV-2 microglia, but I3C did not. DIM, but not I3C, attenuated DNA-binding activity of nuclear factor-κB (NF-κB) and phosphorylation of inhibitor of κB, suggesting that DIM might inhibit microglial hyperactivation by attenuating inflammatory transcription factor NF-κB. In addition, DIM, but not I3C, protected primary cortical neurons from inflammatory toxicity induced by the conditioned media from LPS-stimulated BV-2 microglia, indicating that DIM might attenuate microglial hyperactivation-mediated neuronal death. In an in vivo model of neuroinflammation, DIM suppressed LPS-induced brain inflammation in mouse hippocampus, as determined by the number of Iba-1-positive cells and the mRNA expression of F4/80. Taken together, these results suggest that DIM may have beneficial potential against brain inflammation and neurodegenerative diseases through the negative regulation of the NF-κB signal pathway in microglia.

Keywords: 3; 3′-diindolylmethane; NF-κB; brain inflammation.; cruciferous vegetables; indole-3-carbinol; microglia.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Antigens, Differentiation / genetics
  • Antigens, Differentiation / metabolism
  • Calcium-Binding Proteins / metabolism
  • Cell Death / drug effects
  • Cell Line
  • Culture Media, Conditioned / metabolism
  • Cyclooxygenase 2 / metabolism
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Encephalitis / chemically induced
  • Encephalitis / genetics
  • Encephalitis / metabolism
  • Encephalitis / pathology
  • Encephalitis / prevention & control*
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Hippocampus / pathology
  • Indoles / pharmacology*
  • Lipopolysaccharides*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred ICR
  • Microfilament Proteins / metabolism
  • Microglia / drug effects*
  • Microglia / metabolism
  • Microglia / pathology
  • NF-kappa B / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • RNA, Messenger / metabolism
  • Signal Transduction / drug effects

Substances

  • Aif1 protein, mouse
  • Anti-Inflammatory Agents
  • Antigens, Differentiation
  • Calcium-Binding Proteins
  • Culture Media, Conditioned
  • Indoles
  • Lipopolysaccharides
  • Microfilament Proteins
  • NF-kappa B
  • RNA, Messenger
  • monocyte-macrophage differentiation antigen
  • indole-3-carbinol
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2
  • 3,3'-diindolylmethane