ArticlePloS one2026
Melatonin alleviates chronic intermittent hypoxia-induced gastric mucosal injury via attenuation of oxidative stress and JNK-mediated apoptotic signaling in rats.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTo investigate the mechanism of chronic intermittent hypoxia on gastric injury in rats and the intervening effect and possible mechanism of melatonin.
methodsForty-eight male Wistar rats were randomly divided into normal control, intermittent hypoxia, and melatonin treatment groups. Subgroups (n = 4 per time point) were treated for 2, 4, 6, and 8 weeks. Gastric tissue morphology, gastric juice pH, pepsin levels, oxidative stress markers (MDA and SOD), and the expression of JNK and apoptosis-related genes (Bax, Bcl-2) were assessed.
resultsThe intermittent hypoxia group exhibited significant gastric mucosal damage, decreased pH, increased pepsin, elevated MDA, reduced SOD, and upregulation of JNK and Bax/Bcl-2 mRNA ratio. Melatonin treatment markedly alleviated these pathological and molecular changes compared to the intermittent hypoxia group (P < 0.05).
conclusionChronic intermittent hypoxia induces gastric mucosal injury, which is associated with oxidative stress imbalance and activation of JNK-mediated apoptotic signaling. Melatonin exerts a protective effect by enhancing antioxidant capacity and suppressing the JNK-Bax/Bcl-2 pathway.
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