Background: To investigate the mechanism of chronic intermittent hypoxia on gastric injury in rats and the intervening effect and possible mechanism of melatonin.
Methods: Forty-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.
Results: The 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).
Conclusion: Chronic 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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