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Overview
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Background
Pyrrolidinedithiocarbamate Ammonium is a potent inhibitor of nuclear factor-κB (NF-κB) [1].
NF-κB is a protein complex that controls DNA transcription and cytokine production. It is not only an important factor in regulating inflammation and immune responses and cell survival, but also involved in the cell transformation and tumor formation [1].
In human intestinal epithelial cell line HT-29 induced by interleukin-1β (IL-1β), pretreatment of cells with Pyrrolidinedithiocarbamate Ammonium (3 ~ 1000 μM) dose-dependently attenuated interleukin-8 (IL-8) production. Furthermore, Pyrrolidinedithiocarbamate Ammonium (100 μM) suppressed the accumulation of IL-8 mRNA. Pyrrolidinedithiocarbamate Ammonium inhibited the activation of NF-κB, by suppressing both NF-κB DNA binding and NF-κB-dependent transcriptional activity [2].
In Sprague-Dawley rats pretreated with bacillus Calmette-Guérin (BCG), injection of Pyrrolidinedithiocarbamate Ammonium (50, 100, and 200 mg/kg) reversed hepatic injury stimulated by BCG in vivo. Moreover, Pyrrolidinedithiocarbamate Ammonium inhibited down-regulation of Cytochrome P450 2E1 (CYP2E1) in a dose dependent manner, with ED50 value of 76 mg/kg [1].[1]. Qin J D, Cao Z H, Li X F, et al. Effect of ammonium pyrrolidine dithiocarbamate (PDTC) on NF-κB activation and CYP2E1 content of rats with immunological liver injury. Pharmaceutical Biology, 2014, 52(11): 1460-1466.
[2]. Németh Z H, Deitch E A, Szabó C, et al. Pyrrolidinedithiocarbamate inhibits NF-kappaB activation and IL-8 production in intestinal epithelial cells. Immunology Letters, 2003, 85(1): 41-46.
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