Taurine chloramine (TauCl) is an endogenous anti-inflammatory substance which is derived from
taurine, a semi-essential
sulfur-containing β-
amino acid found in some foods including meat, fish, eggs and milk. In general, TauCl as well as its parent compound
taurine downregulates production of tissue-damaging proinflammatory mediators, such as
chemokines and
cytokines in many different types of cells. In the present study, we investigated the protective effects of TauCl on experimentally induced colon
inflammation.
Oral administration of TauCl protected against mouse
colitis caused by
2,4,6-trinitrobenzene sulfonic acid (TNBS). TauCl administration attenuated apoptosis in the colonic mucosa of TNBS-treated mice. This was accompanied by reduced expression of an oxidative stress marker,
4-hydroxy-2-nonenal and proinflammatory molecules including
tumor necrosis factor-α,
interleukin-6 and
cyclooxygenase-2 in mouse colon. TauCl also inhibited activation of NFκB and STAT3, two key
transcription factors mediating proinflammatory signaling. Notably, the protective effect of TauCl on oxidative stress and
inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding
heme oxygenase-1,
NAD(P)H:
quinone oxidoreductase,
glutamate cysteine ligase catalytic subunit, and
glutathione S-transferase. Taken together, these results suggest that TauCl exerts the protective effect against
colitis through upregulation of Nrf2-dependent cytoprotective gene expression while blocking the proinflammatory signaling mediated by NFκB and STAT3.