The mechanistic action of mogroside V in the alleviation of oxidative aging
Introduce Diseases related to oxidative ageing are becoming increasingly evident in younger individuals. In this study, we investigated the mechanisms underlying the actions of mogroside V when used to treat anti-oxidative ageing.Methods We used D-galactose-induced LO2 cells and C57BL/6J mice as mod...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2025-12-01
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| Series: | Artificial Cells, Nanomedicine, and Biotechnology |
| Subjects: | |
| Online Access: | https://www.tandfonline.com/doi/10.1080/21691401.2025.2486752 |
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| Summary: | Introduce Diseases related to oxidative ageing are becoming increasingly evident in younger individuals. In this study, we investigated the mechanisms underlying the actions of mogroside V when used to treat anti-oxidative ageing.Methods We used D-galactose-induced LO2 cells and C57BL/6J mice as models to investigate the molecular mechanisms of mogroside V (MV) for the treatment of oxidative ageing. Network pharmacology was used to predict the targets of MV for the treatment of oxidative ageing.Results By down-regulating the EGFR/p38/JNK pathway, MV significantly inhibited oxidative ageing and apoptosis in cells, reduced the levels of SA-β-galactosidase. In mice, compared with the model group, MV treatment (100 mg/kg·d) reduced MDA levels and significantly increased the levels of GSH and SOD; furthermore, the size and structure of the liver leaflet and glomeruli was arranged in a regular manner; the small intestine glands had decreased in size. Moreover, the expression levels of Ptp1b mRNA had increased significantly while the levels of c-Jun mRNA and protein were significantly reduced. MV also increased the proportion of beneficial bacteria in the small intestine, including Bacteroidales and Lactobacillaceae.Conclusion Our analyses revealed that MV can significantly reduce oxidative ageing caused by the accumulation of D-galactose. |
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| ISSN: | 2169-1401 2169-141X |