Heme induces oxidative stress and inflammation in gastric epithelial cells via NADPH oxidase activation

Peptic ulcer disease is a prevalent condition that may give rise to several complications, including gastrointestinal bleeding, perforation, and gastric outlet obstruction. Vascular injury during ulceration promotes erythrocyte lysis, resulting in the release of elevated levels of free heme, which can directly interact with the gastric mucosa. Our group has previously demonstrated that heme acts as a pro-inflammatory and pro-oxidative molecule. In this context, oxidative stress has been identified as a central pathogenic mechanism in ulcer progression, leading to cellular dysfunction and tissue injury. In the present study, we investigated the effects of heme on gastric epithelial cell function.