Proliferation in rat gastric mucosal cells induced by chronic ethanol feeding through the ROS/BMK1 pathway

ObjectiveTo 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.MethodsSD 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.ResultsCompared 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.ConclusionThese 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.