Bach1 is a basic region-leucine zipper (bZip) protein that forms heterodimers 
with the small Maf proteins and functions as a repressor of gene expression. One 
of the target genes of Bach1 is Hmox-1 that encodes heme oxygenase-1 (HO-1). 
HO-1 degrades heme into carbon monoxide (CO), biliverdin, and iron. HO-1 is 
strongly induced by various stresses as well as its substrate heme, and protects 
cells and tissues against insults through diverse cytoprotective functions of 
the reaction products CO and biliverdin. Bach1-deficiency in mice leads to 
higher expression of Hmox-1 in various tissues. Here we investigated the effects 
of Bach1-deficiency in mice on tissue injuries: hepatic injury induced by 
D-galactosamine (GalN) and lipopolysaccharide (LPS), and mouse paw edema induced 
by carrageenin, polysaccharide derived from various seaweeds. Bach1-deficiency 
suppressed induction of plasma alanine aminotransferase (ALT) and aspartate 
aminotransferase (AST) activities in response to the GalN/LPS-treatment. 
However, production of tumor necrosis factor alpha (TNF-alpha) and nitric oxide 
(NO), both being cytotoxic mediators in LPS-induced hepatic injury, in 
Bach1-deficient mice and their peritoneal macrophages was similar to wild type 
controls. In contrast, Bach1-deficiency did not affect extent of mouse paw edema 
induced by carrageenin, which enhances vascular permeability by activating kinin 
release. These results indicate that Bach1 plays an inhibitory role in the 
cytoprotection of LPS-induced liver injury but not in the kinin-mediated 
inflammatory edema. The inhibitory role for Bach1 may stem from its activity to 
repress gene expression including HO-1.