Oxidative stress plays an essential role in inflammation and fibrosis. Bach1 is 
an important transcriptional repressor that acts by modulating oxidative stress 
and represents a potential target in the treatment of pulmonary fibrosis (PF). 
In this study, we knocked down Bach1 using adenovirus-mediated small interfering 
RNA (siRNA) to determine whether the use of Bach1 siRNA is an effective 
therapeutic strategy in mice with bleomycin (BLM)‑induced PF. Mouse lung 
fibroblasts (MLFs) were incubated with transforming growth 
factor (TGF)-β1 (5 ng/ml) and subsequently infected with recombined 
adenovirus-like Bach1 siRNA1 and Bach1 siRNA2, while an empty adenovirus vector 
was used as the negative control. The selected Bach1 siRNA with higher 
interference efficiency was used for the animal experiments. A mouse model of 
BLM-induced PF was established, and Bach1 siRNA (1x109 pfu) was administered to 
the mice via the tail vein. The results revealed that the Bach1 mRNA and protein 
levels were significantly downregulated by Bach1 siRNA. Furthermore, the MLFs 
infected with Bach1 siRNA exhibited increased mRNA and protein expression levels 
of heme oxygenase-1 and glutathione peroxidase 1, but decreased levels of TGF-β1 
and interleukin-6 in the cell supernatants compared with the cells exposed to 
TGF-β1 alone. Bach1 knockdown by siRNA also enhanced the expression of 
antioxidant factors, but suppressed that of fibrosis‑related cytokines in mice 
compared with the BLM group. Finally, the inflammatory infiltration of alveolar 
and interstitial cells and the destruction of lung structure were significantly 
attenuated in the mide administered Bach1 siRNA compared with those in the BLM 
group. On the whole, our findings demonstrate that Bach1 siRNA exerts protective 
effects against BLM-induced PF in mice. Our data may provide the basis for the 
development of novel targeted therapeutic strategies for PF.