Inhibition of microRNA-155 regulates gastric mucosal barrier repair and inflammation by targeting SOCS1 for the treatment of acute gastritis.

Acute gastritis is a common gastrointestinal disorder characterized by rapid onset of mucosal injury and infiltration of inflammatory cells, often induced by chemical irritants such as ethanol. Although inflammation is essential for mucosal defense and repair, excessive immune responses can lead to tissue damage and impaired healing. MicroRNAs (miRNAs), particularly those involved in immune regulation, have emerged as important modulators in various inflammatory conditions. However, their specific roles in the early phase of acute gastric inflammation remain unclear, and the mechanisms by which they influence mucosal damage are still not fully understood. In this study, we investigated the expression and functional significance of microRNA-155 (miR-155) in a mouse model of ethanol-induced acute gastritis. Our results showed that miR-155 expression was significantly upregulated in gastric mucosa following ethanol exposure, concomitant with elevated levels of pro-inflammatory cytokines including TNF-α and IL-6. Histological examination revealed that inhibition of miR-155 using a specific antagomir reduced inflammatory cell infiltration and attenuated mucosal injury. These findings suggest that miR-155 contributes to the exacerbation of acute gastric inflammation by promoting cytokine expression and epithelial damage. Importantly, this study highlights the role of miR-155 as an early-response regulator during acute gastric injury. Targeting miR-155 may offer a novel therapeutic strategy for the prevention or treatment of acute gastric mucosal damage. Furthermore, our findings provide a foundation for future exploration of miRNA-based interventions in inflammation-related gastrointestinal diseases.