High-altitude hypoxia exacerbates gastric mucosal damage and regulates the Nrf2 signaling pathway in Helicobacter pylori-infected mice

High-altitude hypoxia exacerbates oxidative stress and inflammatory responses induced by <i>H. pylori</i> infection, reduces tight junction protein expression, and triggers changes in apoptosis-related protein expression, exacerbating the disruption of the gastric mucosal barrier, consequently leading to more severe gastric mucosal damage. The underlying mechanism may be associated with the inhibition of the Nrf2 signaling pathway in the gastric tissues.