ArticleJournal of ginseng research2026
Total saponins from
Article in Journal of ginseng research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
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Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Aging, as an inevitable biological process, is an inevitable process of multisystem functional decline, with cellular senescence being one of its hallmarks. Although total saponins from Methods: A rapid dual-system screening model of aging was established using tert-butyl hydrogen peroxide (tBHP) to induce senescence in human umbilical vein endothelial cells (HUVECs) and Results: TSG alleviated oxidative stress, enhanced antioxidant capacity and reduced β-galactosidase activity, indicating delayed aging. It also modulated senescence-related markers and increased Ki-67, supporting its role in promoting proliferation and suppressing cellular senescence. Among 20 ginsenosides screened, PPD, F1 and Rh1 were identified as the principal active components. Network pharmacology and experimental validation revealed the PI3K-AKT pathway as central to TSG's effects. AKT1 and PI3K were confirmed as the targets, with decreased phosphorylation levels observed. TSG's anti-aging effects were partly abolished in loss-of-function mutant worms Conclusion: This study establishes a rapid dual-system model for aging research, and demonstrates that TSG and its principal ginsenosides (PPD, F1 and Rh1) mitigate aging and cellular senescence through the PI3K-AKT pathway by downregulating PI3K/AKT phosphorylation.
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Registered trials
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