Vitamin E Inhibits Oxidative Stress and Inflammation in Stress‐Induced Gastritis via Modulating Nrf2 and NF‐κB Signalling Pathways

The incidence of stress-induced gastritis is gradually increasing. Vitamin E (VE) is widely used in inflammatory diseases due to its efficient antioxidant and anti-inflammatory effects. Here, we investigated the protective role of VE on stress-induced gastritis and its potential mechanisms. Mice were subjected to high-intensity stress caused by the forced swim test (FST) and gavaged with VE (300 mg/kg) at different time points. The results showed that VE significantly alleviated stress-induced gastric mucosal injury and related histopathological changes. Additionally, the expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), haem oxygenase-1 (Hmox1) and NAD(P)H:quinone oxidoreductase 1 (NQO1) were upregulated in the administrated groups, while the nuclear factor kappa B (NF-κB) signalling pathway was inhibited, manifested as the expression level of p-NF-κB p65 protein decreased. Furthermore, VE reduced the infiltration of macrophages in gastric tissue, followed by a synchronous decrease in the expression level of interleukin-1 beta (IL-1β) protein. Importantly, the detection of cell death by TUNEL assay and SYTOX green staining demonstrated that VE reduced cell death of gastric tissue and subsequently downregulated the pro-apoptotic factor BCL2-associated X Protein (Bax). Hence, our study suggested that VE has an outstanding preventive and therapeutic effect on stress-induced gastritis via promoting Nrf2 and inhibiting NF-κB signalling.