ZHANG Huie, DU Lianyun, CHU Mengyao, et al. Ginseng Folium Attenuates Skin Aging by Limiting the Accumulation of Cellular Reactive Oxygen Species[J]. Science and Technology of Food Industry, 2024, 45(3): 328−337. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2023030042.
Citation: ZHANG Huie, DU Lianyun, CHU Mengyao, et al. Ginseng Folium Attenuates Skin Aging by Limiting the Accumulation of Cellular Reactive Oxygen Species[J]. Science and Technology of Food Industry, 2024, 45(3): 328−337. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2023030042.

Ginseng Folium Attenuates Skin Aging by Limiting the Accumulation of Cellular Reactive Oxygen Species

  • Objective: A network pharmacology-based approach, molecular docking and in vitro experimental validation were performed to reveal bioactive compounds and the molecular mechanism of ginseng folium via treating UVB-induced skin aging. Methods: The active components and targets of ginseng folium were obtained by TCMSP, and skin aging-related targets were retrieved by GeneCards and OMIM. Online Venn diagram was used to obtain the intersection targets. Cytoscape 3.7.0 software was used to conduct a comprehensive visual analysis of the multi-level network data of 'drug-component-target-disease'. DAVID database was used to perform GO and KEGG enrichment analysis on the common targets. AutoDock docked the drugs to the predicted drug binding sites. The oxidative damage-related indicators and protein expression levels of HaCaT cells during UVB irradiation-induced senescence were detected in vitro. Results: As a result, four active components (sitosterol, quercetin, ginsenoside Rh2 and kaempferol) of ginseng folium and the 94 potential targets were predicted. The ginseng folium could significantly reduce the oxidative damage of the HaCaT aging model induced by UVB radiation, the same as the expression of p-JNK, and p-ERK proteins. Conclusion: Sitosterol, quercetin, ginsenoside Rh2, kaempferol, and other components in ginseng folium could activate the MAPK, PI3K/Akt, and other signal pathways through p-JNK, p-ERK, and other proteins to inhibit the production of lipid peroxides, protection on HaCaT cells, achieve multi-components, multi-targets, multi-channel effects, and resist the appearance and progress of skin aging.
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