In the current study, HCl/ethanol treatment suppressed HO-1 expression, which was consistent with the result of Ueda et al. [49], in which HO-1 inhibition results in increased acute gastric mucosal lesions and Gomes et al. [50] documented that HO-1/biliverdin/CO pathway played a cytoprotective role against ethanol-induced gastropathy and that these defensive effects probably result from decreased free radical generation. Here, HMOX1 is linked to stomach disorder.