In experimental models of colitis, specifically in groups treated with DSS (dextran sulfate sodium) and pyrrolidinedithiocarbamate ammonium, there was observed suppression in the shortening of intestinal length and a reduction in the DAI (Disease Activity Index) score. Moreover, levels of activated NF-κB, IL-1β, and TNF-α were significantly lower in the DSS+pyrrolidinedithiocarbamate ammonium-treated group, suggesting that inhibiting NF-κB activity with this compound can delay the healing of mucosal tissue defects, such as erosions or ulcers, caused by inflammation. However, it can significantly suppress the expression of inflammatory cytokines (IL-1β and TNF-α), thus considerably alleviating symptoms of colitis. These properties highlight the potential of pyrrolidinedithiocarbamate ammonium in treating ulcerative colitis^[2].

Pyrrolidinedithiocarbamate ammonium, ranging from 3 to 1000 μM, when used as a pretreatment, dose-dependently reduces IL-8 production in cells^[1].

Pyrrolidinedithiocarbamate ammonium functions by inhibiting the activation of NF-κB, effectively diminishing both NF-κB DNA binding and its dependent transcriptional activity. Consequently, the inhibition of NF-κB with pyrrolidinedithiocarbamate ammonium results in decreased IL-8 production by intestinal epithelial cells, underscoring its mechanism of action^[1].