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Abstract Ethanol-induced gastric injury is a prevalent clinical issue characterized by oxidative stress, inflammation, and apoptosis in gastric epithelial cells. Luteolin, a naturally occurring flavonoid with potent antioxidant and anti-inflammatory properties, has shown promise as a therapeutic agent for managing such damage. This study explores the protective effects of luteolin on ethanol-induced injury in gastric epithelial cells (GES-1) and investigates the underlying mechanisms, with a focus on the Keap1/Nrf2 signaling pathway. Our findings demonstrate that luteolin significantly enhances cell viability, reduces lactate dehydrogenase (LDH) release, and helps maintain mitochondrial membrane potential (MMP) in ethanol-treated cells. Luteolin also mitigates oxidative stress by increasing the activity of antioxidant enzyme activities (CAT, SOD) and glutathione (GSH) levels and decreasing malondialdehyde (MDA) levels. Additionally, it suppresses inflammation by reducing the expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and inhibits apoptosis by modulating the expression of Bax, caspase-3, and Bcl-2. Mechanistically, luteolin activates the Keap1/Nrf2 signaling pathway, which restores redox balance and reduces inflammation, highlighting its central role in luteolin’s protective effects. These results provide valuable insights into the therapeutic potential of luteolin in addressing alcohol-related gastric injuries and oxidative stress-driven disorders, offering a mechanistic basis for its application in clinical settings.
Zhu et al. (Mon,) studied this question.