BTB and CNC homolog 1 (Bach1) is a transcriptional repressor of heme oxygenase-1 
(HO-1). It plays an important role in the feedback regulation of HO-1 
expression, which protects cells from various insults including oxidative stress 
and inflammatory cytokines. However, the role of Bach1 in intestinal 
inflammation remains unclear. In this study, the role of Bach1 in intestinal 
mucosal injury was elucidated using 8-week-old female C57BL/6 (wild-type) and 
homozygous Bach1-deficient C57BL/6 mice. Intestinal mucosal injuries induced by 
a single subcutaneous administration of indomethacin were evaluated 
macroscopically, histologically, and biochemically. Mucosal protein content and 
chemokine mRNA levels were determined by real-time PCR. Our results showed that 
the indomethacin-induced intestinal injury was remarkably improved in 
Bach1-deficient mice. Histological examination showed that the area of injured 
lesion was decreased in Bach1-deficient mice compared to wild-type mice. 
Administration of indomethacin induced expression of inflammatory chemokines 
such as KC, MIP1alpha and MCP1, which was suppressed in Bach1-deficient mice. 
Myeloperoxidase activity in the intestinal mucosa was also significantly 
decreased in Bach1-deficient mice. Additionally, Bach1 deficiency enhanced 
immunopositivity of HO-1 in the intestinal mucosa after indomethacin 
administration. Disruption of the Bach1 gene thus caused inhibition of mucosal 
injury, indicating that inhibition of Bach1 may be a novel therapeutic strategy 
for treating indomethacin-induced intestinal injury.