The DSS+pyrrolidinedithiocarbamate ammonium-treated groupII exhibits suppression of shortening of intestinal length and reduction of DAI score. Activated NF-κB level and IL-1β and TNF-α levels are significantly lower in DSS+pyrrolidinedithiocarbamate ammonium-treated groupII. These findings suggest that suppression of NF-κB activity by pyrrolidinedithiocarbamate ammonium can delay the healing of mucosal tissue defects (erosions or ulcers) arising from inflammation, but that it can strongly suppress the expression of inf-lammatory cytokines (IL-1β and TNF-α), resulting in significant alleviation of colitis. pyrrolidinedithiocarbamate ammonium is useful for the treatment of ulcerative colitis[2].
In Vitro
Pretreatment of cells with pyrrolidinedithiocarbamate (3-1000 μM) dose-dependently attenuate IL-8 production. Furthermore, pyrrolidinedithiocarbamate (100 μM) suppresses the accumulation of IL-8 mRNA. Pyrrolidinedithiocarbamate inhibits the activation of NF-κB, because pyrrolidinedithiocarbamate suppresses both NF-κB DNA binding and NF-κB-dependent transcriptional activity. NF-κB inhibition with pyrrolidinedithiocarbamate decrease IL-8 production by intestinal epithelial cells[1].
Kinase Assay
Cell Assay
Animal Administration
References
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