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Diallyl trisulfide inhibits tumor necrosis factor-alpha expression in inflammed mucosa of ulcerative colitis

Ai-Ping Bai1, Qin Ouyang, Ren-Wei Hu

  • 1Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou City 510080, China. baiap@163.com

Digestive Diseases and Sciences
|August 23, 2005
PubMed

Insights

Diallyl trisulfide (DATS) reduces tumor necrosis factor-alpha (TNF-alpha) in ulcerative colitis. This compound inhibits NF-kappaB activation in inflamed colonic tissue without affecting cell viability.

Area of Science:

  • Gastroenterology
  • Immunology
  • Pharmacology

Background:

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease.
  • Tumor necrosis factor-alpha (TNF-alpha) plays a key role in UC pathogenesis.
  • NF-kappaB signaling pathway is a critical regulator of TNF-alpha production.

Purpose of the Study:

  • To investigate the effect of diallyl trisulfide (DATS) on TNF-alpha expression in UC.
  • To elucidate the underlying mechanism of DATS action in inflamed colonic mucosa.

Main Methods:

  • Colonic biopsies from UC patients were treated with varying concentrations of DATS (0-10 microM).
  • TNF-alpha levels, lactate dehydrogenase (LDH) activity, TNF-alpha mRNA expression, and NF-kappaB P65 activation were assessed.
  • RT-PCR and immunohistochemistry were employed to analyze gene and protein expression.

Main Results:

  • DATS treatment (5 and 10 microM) significantly reduced TNF-alpha concentrations in supernatants.
  • 10 microM DATS decreased TNF-alpha mRNA expression and NF-kappaB P65 nuclear translocation in lamina propria mononuclear cells.
  • LDH activity remained unchanged, indicating no DATS-induced cytotoxicity.

Conclusions:

  • DATS effectively downregulates TNF-alpha production in inflamed UC mucosa.
  • DATS inhibits NF-kappaB activation in colonic cells, suggesting a therapeutic potential for UC.
  • DATS demonstrates a favorable safety profile regarding colonic tissue viability.

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