吡咯烷二硫代甲酸铵盐

Pretreatment of cells with Pyrrolidinedithiocarbamate ammonium (Ammonium pyrrolidinedithiocarbamate; 3-1000 μM) dose-dependently attenuate IL-8 production.
Furthermore, pyrrolidinedithiocarbamate ammonium (100 μM) suppresses the accumulation of IL-8 mRNA.
Pyrrolidinedithiocarbamate ammonium inhibits the activation of NF-κB, because it suppresses both NF-κB DNA binding and NF-κB-dependent transcriptional activity. NF-κB inhibition with pyrrolidinedithiocarbamate ammonium decrease IL-8 production by intestinal epithelial cells.

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.