Heme oxygenase‐1: a new therapeutic target for inflammatory bowel disease

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Abstract
Heme oxygenase (HO) is the rate‐limiting enzyme in the catabolism of heme, followed by production of biliverdin, free iron and carbon monoxide (CO). Three mammalian HO isozymes have been identified, one of which, HO‐1, is a stress‐responsive protein induced by various oxidative agents. HO‐2 and HO‐3 genes are constitutively expressed. Recent studies demonstrate that the expression of HO‐1 in response to different inflammatory mediators may contribute to the resolution of inflammation and have protective effects in several organs against oxidative injury. Although the mechanism underlying the anti‐inflammatory actions of HO‐1 remains poorly defined, both CO and biliverdin/bilirubin have been implicated in this response. In the intestinal tract, HO‐1 is shown to be transcriptionally induced in response to oxidative stress, preconditioning and acute inflammation. Recent studies suggest that the induction of HO‐1 expression plays a critical protective role in intestinal damage models induced by trinitrobenzene sulphonic acid or dextran sulphate sodium, indicating that activation of HO‐1 may act as an endogenous defensive mechanism to reduce inflammation and tissue injury in the intestinal tract. These in vitro and in vivo data suggest that HO‐1 may be a novel therapeutic target in patients with inflammatory bowel disease.

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