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Combined Metabolomics to Reveal the Beneficial Efficacy and Mechanism of Ripe Pu‐erh Tea in Alleviating Alcohol‐Induced Acute Gastric Injury in Mice
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Combined Metabolomics to Reveal the Beneficial Efficacy and Mechanism of Ripe Pu‐erh Tea in Alleviating Alcohol‐Induced Acute Gastric Injury in Mice
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Journal Article
Combined Metabolomics to Reveal the Beneficial Efficacy and Mechanism of Ripe Pu‐erh Tea in Alleviating Alcohol‐Induced Acute Gastric Injury in Mice
2025
Overview
The protective effects of ripe Pu‐erh tea extract (PTE) against alcohol‐induced gastric injury were investigated through in vitro analysis, animal treatments, and nontargeted metabolomic analysis. In this study, in vitro analysis revealed that catechins were altered during digestive phases, whereas gallocatechin and gallic acid persisted until the intestinal period. In vitro antioxidant capacity of PTE could be maintained until the stage of gastric digestion. In acute alcohol‐exposed mice, PTE prevented alcohol‐induced gastric injury, which was characterized by significant reduction of gastric ulcer index. The gastric barrier integrity (PGE2, Muc2, Occludin and ZO‐1) was restored in PTE‐treated mice. The alcohol‐induced decreasing trends of antioxidant enzymatic activities (SOD and GSH) were significantly reversed by PTE, which was associated with the activation of oxidative stress pathways (Keap1/Nrf2/HO‐1). Besides, PTE reduced the levels of pro‐inflammatory cytokines (IL‐6, IL‐1β, and TNF‐α), likely owing to the inhibition of the NF‐κB pathway. Furthermore, nontargeted metabolomics identified elevated levels of anti‐inflammatory bile acids (e.g., hyodeoxycholic acid) in PTE‐treated mice, suggesting ethanol‐induced inflammation might be ameliorated by PTE through modulation of bile acid metabolism. Overall, PTE could be a functional beverage for treating acute alcohol consumption‐induced gastric injury and metabolomic disorders. PTE ameliorates alcohol‐induced gastric injury by regulating oxidative stress and inflammatory responses. Activation of the Keap1/Nrf2/HO‐1 pathway and suppression of NF‐κB pathway may represent the molecular mechanisms by which PTE mediates antioxidative and anti‐inflammatory effects.
Publisher
John Wiley & Sons, Inc,Wiley
Subject
