ArticleJournal of ginseng research2026
Anti-skin aging effects of black ginseng extracts through regulating inflammatory factors and the CLOCK-ERK pathway in mice.
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. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Ginsenoside Rb2 modulates the skin barrier by targeting Src to regulate PI3K/Akt signaling in HaCaT cells.Journal of ginseng research · 2026Article
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8 authors.
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Abstract
Background: Continuous light exposure can accelerate immunosenescence-like state. The increase of TNF-α and IL-1β impairs clock gene functions and circadian rhythm disorder contributes to the path of biological aging. Methods: This study evaluated the effects of an aqueous extract of black ginseng (BG) on clock gene regulation in aging mice accompanied by circadian rhythm disorders to clarify its antiaging mechanism in the skin. D-gal-induced the mouse embryonic fibroblast (MEF) cells were treated with Ginsenoside Rg3. In vivo, aging senescence was induced by subcutaneous injection of D-gal combined with a light environment. The treatment groups were injected intraperitoneally with BG extract. Results: We found that Rg3, one of the active ingredients of the BG extract, increased the antioxidant capacity and decreased the expression of β-galactosidase and the mRNA levels of p16, p21, TNF-α and IL-1β. Drug-disease-target network pharmacological analysis revealed that the TNF signaling pathway is involved in the anti-skin aging effects of both BG and PT. We verified that BG or PT reversed the changes in the levels of IL-1β, TNF-α, clock and p-ERK1/2 in aged and circadian rhythm-disturbed mice. Conclusions: The present study demonstrated that the extracts of BG and PT played similar roles in an anti-skin aging. The possible mechanism involves the inhibition of oxidative stress (OS) and inflammation, which can lead to change clock genes and drive epidermal differentiation of epidermal stem cells (ESCs) through the activation of ERK to cause ESCs depletion and skin aging.
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