Inflammatory bowel disease is associated with chronic abdominal pain. Transient receptor potential ankyrin 1 (TRPA1) is a well‐known pain sensor expressed in primary sensory neurons. Recent studies indicate that reactive oxygen species such as hydrogen peroxide (H₂O₂) may activate TRPA1.

Colonic inflammation was induced by intra‐colonic administration of trinitrobenzene sulfate (TNBS) in adult male Sprague–Dawley rats. Visceromotor response (VMR) to colorectal distention (CRD) was recorded to evaluate the visceral hyperalgesia. Rats were sacrificed 1 day after treatment with saline or TNBS; colonic tissues from the inflamed region were removed and then processed to assess the H₂O₂ content. H₂O₂ scavenger N‐acetyl‐l‐cysteine or a TRPA1 antagonist, HC‐030031, was intravenously administrated to the TNBS‐treated rats or saline‐treated rats. In a parallel experiment, intra‐colonic H₂O₂‐induced visceral hyperalgesia in naïve rats and the effect of intravenous HC‐030031 were measured based on the VMR to CRD.

Trinitrobenzene sulfate treatment resulted in significant increase in VMR to CRD at day 1. The H₂O₂ content in the inflamed region of the colon in TNBS‐treated rats was significantly higher than that of saline‐treated rats. N‐acetyl‐l‐cysteine or HC‐030031 significantly suppressed the enhanced VMR in TNBS‐treated rats while saline‐treated rats remained unaffected. Moreover, blockade of TRPA1 activation by HC‐030031 significantly reversed the exogenous H₂O₂‐induced visceral hyperalgesia.

These results suggest that H₂O₂ content of the colonic tissue is increased in the early stage of TNBS‐induced colitis. The increased H₂O₂ content may contribute to the visceral hyperalgesia by activating TRPA1.