Upregulated miRNA may be responsible for the development of intestinal inflammation in UC.

Taken together, the results indicated that the inhibition of endogenous H(2)S generation caused the deterioration of DSS-induced colitis. We conclude that physiological H(2)S might act as an anti-inflammatory molecule in colitis.

The protective effect of PZ on indomethacin-induced small intestinal injury may be dependent on its ROS-quenching effect.

The inhalation of CO protected mice from developing intestinal inflammation. Based on these data, the beneficial effects of CO in a murine colitis model may be attributed to its anti-inflammatory properties.

Taken together, reactive oxygen species production is one of the mechanisms by which indomethacin induced small intestinal injury.