Journal of ethnopharmacology · 2025
Ampelopsis grossedentata protects against ethanol-induced acute duodenal injury by inhibiting TNF-triggered caspases-dependent apoptosis in mice.
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Sun Chao-Yue, Li Wan-Qing, Lu Jing-Wen, Zhang Ao-Yue, Chu Qing-Xia, Tang Li, Gao Wei, Cai Jin-Jie, Lu Ying, Liu Dong
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Ampelopsis grossedentata (AG) is a popular folk tea that has been used in China for more than 1000 years. It is noteworthy that AG is widely recognized for preventing alcohol hangover in folk, and its protective effects on alcohol-induced hepatic steatosis have been demonstrated.
AIM OF THE STUDY: Alcohol overconsumption can induce acute duodenal injury (ADI) that lacks effective therapeutic strategies. This study investigated the gastrointestinal protective effects of AG on alcoholic ADI in mice.
MATERIALS AND METHODS: AG extract was chemically characterized by HPLC analysis. Institute of Cancer Research (ICR) mice were pre-administered AG extract via gavage, and then subjected to an ethanol-induced ADI. After treatment, duodenal tissues were stained with hematoxylin and eosin (H&E), and cell apoptosis was detected by TUNEL staining and immunofluorescence. Untargeted metabolomics was employed to identify the differentially expressed metabolites, and the gene expressions of duodenal tissues were determined using RNA sequencing, immunofluorescence, immunohistochemistry, and western blotting.
RESULTS: Acute ethanol administration caused severe duodenal damage, characterized by necrosis and shedding of duodenal villi, hemorrhagic injury, mucosal edema, and disruption of intestinal barrier in mice, which was improved by the pre-treatment with AG extract. Notably, administration of AG aqueous extract suppressed ethanol-induced duodenal villous apoptosis in mice by inhibiting caspase-3/7. In addition, untargeted metabolomics data showed AG extract improved ethanol-induced disruption of amino acid biosynthesis and metabolism, and increased the levels of amino acids, such as L-serine, L-histidine, L-leucine, L-glutamine and L-tryptophan. RNA sequencing analysis revealed that ethanol intake activated TNF, IL-17, MAPK and apoptosis pathways, and these pathways were inhibited by AG extract pre-treatment. Immunofluorescence and immunohistochemistry results showed AG extract reduced the expressions of TNF-a, FADD, TRADD, RIPK1 and caspase-8 activity in duodenal tissue in ethanol-fed mice. In addition, western blotting data showed that pre-treatment with AG extract suppressed ethanol-induced activation of IL-17 and MAPK pathways.
CONCLUSION: In conclusion, pre-treatment with AG inhibited ethanol-induced apoptosis of duodenal villi, disruption of intestinal barrier and amino acids metabolic disturbance. AG extract inhibited the TNF-a/FADD/caspase-8 and IL-17/MAPK signaling pathways. These findings highlight the gastrointestinal protective effects of AG extract against alcoholic ADI, and support its application as a duodenal protectant in drug development and dietary supplements.
AIM OF THE STUDY: Alcohol overconsumption can induce acute duodenal injury (ADI) that lacks effective therapeutic strategies. This study investigated the gastrointestinal protective effects of AG on alcoholic ADI in mice.
MATERIALS AND METHODS: AG extract was chemically characterized by HPLC analysis. Institute of Cancer Research (ICR) mice were pre-administered AG extract via gavage, and then subjected to an ethanol-induced ADI. After treatment, duodenal tissues were stained with hematoxylin and eosin (H&E), and cell apoptosis was detected by TUNEL staining and immunofluorescence. Untargeted metabolomics was employed to identify the differentially expressed metabolites, and the gene expressions of duodenal tissues were determined using RNA sequencing, immunofluorescence, immunohistochemistry, and western blotting.
RESULTS: Acute ethanol administration caused severe duodenal damage, characterized by necrosis and shedding of duodenal villi, hemorrhagic injury, mucosal edema, and disruption of intestinal barrier in mice, which was improved by the pre-treatment with AG extract. Notably, administration of AG aqueous extract suppressed ethanol-induced duodenal villous apoptosis in mice by inhibiting caspase-3/7. In addition, untargeted metabolomics data showed AG extract improved ethanol-induced disruption of amino acid biosynthesis and metabolism, and increased the levels of amino acids, such as L-serine, L-histidine, L-leucine, L-glutamine and L-tryptophan. RNA sequencing analysis revealed that ethanol intake activated TNF, IL-17, MAPK and apoptosis pathways, and these pathways were inhibited by AG extract pre-treatment. Immunofluorescence and immunohistochemistry results showed AG extract reduced the expressions of TNF-a, FADD, TRADD, RIPK1 and caspase-8 activity in duodenal tissue in ethanol-fed mice. In addition, western blotting data showed that pre-treatment with AG extract suppressed ethanol-induced activation of IL-17 and MAPK pathways.
CONCLUSION: In conclusion, pre-treatment with AG inhibited ethanol-induced apoptosis of duodenal villi, disruption of intestinal barrier and amino acids metabolic disturbance. AG extract inhibited the TNF-a/FADD/caspase-8 and IL-17/MAPK signaling pathways. These findings highlight the gastrointestinal protective effects of AG extract against alcoholic ADI, and support its application as a duodenal protectant in drug development and dietary supplements.