Le Carbone, a charcoal supplement, modulates DSS-induced acute colitis in mice through activation of AMPKα and downregulation of STAT3 and caspase 3 dependent apoptotic pathways

Int Immunopharmacol. 2017 Feb:43:70-78. doi: 10.1016/j.intimp.2016.10.023. Epub 2016 Dec 12.

Abstract

Le Carbone (LC) is a charcoal supplement, which contains a large amount of dietary fibers. Several studies suggested that charcoal supplement may be beneficial for stomach disorders, diarrhea, gas and indigestion. But no studies address whether LC intake would suppress inflammation, cell proliferation or disease progression in colitis. In the present study, the effect of LC on experimental colitis induced by dextran sulfate sodium (DSS) in mice and its possible mechanism of action were examined. A study was designed for 8days, using C57BL/6 female mice that were administered with 3% DSS in drinking water for 7days followed by another 1day consumption of normal water with or without treatment. LC suspension was administered daily for 7days via oral gavage using 5mg/mouse in treatment group and normal group was supplied with drinking water. LC suspension significantly attenuated the loss of body weight and shortening of colon length induced by DSS. The disease activity index, histopathologic changes were significantly reduced by LC treatment. The inflammatory mediators TNFα, IL-1β, p-STAT3 and p-NF-κB induced in the colon by DSS were markedly suppressed by LC. The increased activation of AMPKα in the colon was also detected in LC group. Furthermore, the apoptotic marker protein cleaved caspase 3 was down-regulated and anti-apoptotic proteins Bcl2 and Bcl-xL were significantly up-regulated by LC treatment. Taken together, our results demonstrate the ability of LC to inhibit inflammation, apoptosis and give some evidence for its potential use as adjuvant treatment of inflammatory bowel disease.

Keywords: AMPKα; Apoptosis; Bcl2; Colitis; Dietary supplement; IL-1β; Le Carbone; TNFα.

MeSH terms

  • AMP-Activated Protein Kinases / metabolism*
  • Acute Disease
  • Animals
  • Anti-Inflammatory Agents / therapeutic use*
  • Apoptosis / drug effects
  • Caspase 3 / genetics
  • Caspase 3 / metabolism*
  • Charcoal / therapeutic use*
  • Colitis / chemically induced
  • Colitis / drug therapy*
  • Colon / drug effects*
  • Colon / pathology
  • Dextran Sulfate
  • Female
  • Humans
  • Interleukin-1beta / metabolism
  • Mice
  • Mice, Inbred C57BL
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism*
  • Signal Transduction / drug effects
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Interleukin-1beta
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Tumor Necrosis Factor-alpha
  • Charcoal
  • Dextran Sulfate
  • AMPK alpha1 subunit, mouse
  • AMP-Activated Protein Kinases
  • Caspase 3