Objective: To investigate the correlation between the gastric mucosal cell proliferation and low-concentration alcohol intake in a chronic drinking rat model

and to investigate the possible role of ROS/BMK1 pathway in this process. Methods: SD rats were randomly divided into 4 groups: control group

administered with tap water; ethanol group

with 6% ethanol in the drinking water; quercetin group

with quercetin （100 mg/kg） by intragastric gavage twice a day; ethanol+quercetin group

administered with quercetin combined with 6% ethanol. The cell proliferation in rat gastric mucosa was analyzed by flow cytometery and proliferating cell nuclear antigen （PCNA） immunohistochemical staining. Activation of ERKs and BMK1 was evaluated by the expression and phosphorylation of these kinases using Western Blot analysis. Results: Compared to the controls

the cell proliferation in gastric mucosa of rats exposed to the ethanol for 7 d was enhanced

and the activation of BMK1 was also increased in this period. Otherwise quercetin

as a free radical scavenger

attenuated increased cell proliferation and activation of BMK1 in rat stomach treated with ethanol. However

no changes of ERKs expression and phosphorylation occurred in the rats in all groups. Conclusion: These results suggested that the ROS and BMK1 activation may be a central mechanism

which underlies cell proliferation in rat gastric mucosa stimulus with the chronic low-concentration ethanol.