Bach1 is a transcriptional repressor of heme oxygenase-1 (HO-1, a.k.a. HSP-32), 
which is an inducible enzyme and has anti-oxidation/anti-inflammatory properties 
shown in various models of organ injuries. Since oxidative stress plays a 
pivotal role in the pathogenesis of nonalcoholic steatohepatitis (NASH), HO-1 
induction would be expected to prevent the development of NASH. In this study, 
we investigated the influence of Bach1 ablation in mice on the progression of 
NASH in methionine-choline deficient (MCD) diet model. Bach1 ablation resulted 
in significant induction of HO-1 mRNA and its activity in the liver. When fed 
MCD diet, Bach1(-/-) mice exhibited negligible hepatic steatosis compared to 
pronounced steatohepatitis in wild type mice with 6-fold increase in hepatic 
triglyceride content. Whereas feeding of MCD diet decreased mRNA expressions of 
peroxisome proliferator-activated receptor (PPAR) α and microsomal triglyceride 
transfer protein (MTP) in wild type mice, there were no change in Bach1(-/-) 
mice. In addition, hepatic concentration of malondialdehyde (MDA), a biomarker 
for oxidative stress as well as plasma alanine aminotransferase (ALT) was 
significantly lower in Bach1(-/-) mice. These findings suggest that Bach1 
ablation exerts hepatoprotective effect against steatohepatitis presumably via 
HO-1 induction and may be a potential therapeutic target.