Diallyl Trisulfide Inhibits Tumor Necrosis Factor-α Expression in Inflammed Mucosa of Ulcerative Colitis

Abstract

The present study aimed to investigate the effect of diallyl trisulfide (DATS) on tumor necrosis factor (TNF)-alpha expression in inflammed mucosa of ulcerative colitis and its possible mechanism. Colonic biopsies from ulcerative colitis were treated with 0, 1, 5, and 10 microM DATS for 24 hr. Lactate dehydrogenase (LDH) activities and concentrations of TNF-alpha in supernatants were measured. mRNA expressions of TNF-alpha in biopsies were analyzed by RT-PCR. The expression of NF-kappaB P65 in tissues was studied by immunohistochemistry. Concentrations of TNF-alpha in supernatants of biopsies treated with 5 and 10 microM DATS were lower than those of untreated biopsies. There were fewer lamina propria mononuclear cells whose NF-kappaB P65 expression in nuclei was positive, and less mRNA expression of TNF-alpha in biopsies treated with 10 microM DATS than in untreated biopsies. There were no differences in LDH activities in supernatants between tissues treated with DATS and untreated tissues. DATS could downregulate TNF-alpha production and inhibit NF-kappaB activation in lamina propria mononuclear cells of inflammed mucosa, without any effect on the viability of colonic tissue cells.

Endogenous and Exogenous Hydrogen Sulfide Promotes Resolution of Colitis in Rats

“…Previously, a garlic-derived substance that releases H 2 S (allyl trisulfide) 37 was shown to suppress TNF-␣ expression and NF-B activation in colonic biopsy samples from ulcerative colitis patients. 38 We also observed that an inhibitor of H 2 S synthesis markedly down-regulated colonic COX-2 activity, and this was accompanied by reduced colonic prostaglandin E 2 synthesis and induction of inflammation in the tissue. COX-2 is a source of several antiinflammatory eicosanoids and plays a crucial role in the resolution of inflammation in many tissues, 39 -41 including the gastrointestinal tract.…”

Tanshinone IIA Ameliorates Trinitrobenzene Sulfonic Acid (TNBS)-Induced Murine Colitis

“…Many researches are pursuing potent new drugs for IBD management. To date, a lot of papers have reported that some components of vegetables and herbs can inhibit the inflammatory response of IBD or experimental colitis [4][5][6], and show new potential therapeutics for IBD in future.…”

Cytoprotective Effects of Hydrogen Sulfide in Novel Rat Models of Non-Erosive Esophagitis

“…However, there is substantial evidence that H 2 S is produced throughout the GI tract and it participates in many physiological functions in addition to promoting mucosal integrity, reducing mucosal inflammation and accelerating healing of ulcers [28] – [30] , [34] , [38] . Accleration of ulcer healing is most likely related to the ability of H 2 S to promote angiogenesis [30] , [39] , while prevention of tissue injury may be related to the ability of H 2 S to maintain mucosal blood flow [29] , [38] , stimulate bicarbonate secretion [40] , [41] , stimulate mucus secretion [42] , inhibit leukocyte adherence to the vascular endothelium [43] , scavenge free radicals [44] , promote resolution of inflammation by increasing neutrophil apoptosis [45] and differentiation of macrophages to the M2 phenotype [46] , and suppress production of pro-inflammatory cytokines (including IL-1, IL-2, IL-8 and TNFα) [47] – [50] , while maintaining or increasing production of IL-10 [47] – [50] . Suppression of IL-8 production in keratinocytes by H 2 S has been reported to be a consequence of diminished IL-17 production, as IL-17 can induce IL-8 production [51] , [52] .…”