Signal transduction and targeted therapyOct 28, 2026

Ginsenoside Rb1 may reduce uterine aging by blocking a key cell growth pathway

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Oct 29, 2026

Abstract

Rb1 treatment can attenuate oxidative stress, senescence, and apoptosis in endometrial stromal cells of aging uterine tissue.

Uterine aging is linked to defective endometrial decidualization and implantation failure.
Cellular senescence in endometrial stromal cells is a significant factor driving uterine aging.
Rb1 has been shown to alleviate cellular senescence by suppressing oxidative and inflammatory pathways.
Proteomic analysis indicates that Rb1 regulates pathways related to the mammalian target of rapamycin (mTOR).
Rb1 activates AMP-activated protein kinase (AMPK), which helps suppress the mTOR-NF-κB signaling loop.
Rb1 targets senescence-associated dysfunction, potentially restoring endometrial homeostasis.

Simplified

Uterine aging impairs fertility and reproductive health, but the underlying pathogenic mechanisms and effective treatment strategies remain elusive. Defective endometrial decidualization and implantation failure are hallmarks of uterine aging, which can be driven by cellular senescence, especially in endometrial stromal cells (EnSCs). Rb1 has been reported to relieve cellular senescence by suppressing oxidative and inflammatory pathways. However, whether Rb1 functions in alleviating uterine aging remains uncertain. Here, we demonstrate that Rb1 can attenuate oxidative stress, senescence, and apoptosis in the EnSCs of the aging human endometrium and murine uterus. Further proteomic analysis reveals that Rb1 safeguards against endometrial aging by regulating mammalian target of rapamycin (mTOR)-related pathways. Rb1 treatment results in the activation of AMP-activated protein kinase (AMPK) and AMPK-mediated suppression of the mTOR-nuclear factor-kappa B (NF-κB) signaling loop, thereby ameliorating aging-related phenotypes. Collectively, our findings illustrate that Rb1 alleviates uterine aging by attenuating endometrial stromal cell senescence and suppressing AMPK-mTOR-NF-κB-driven inflammatory signaling. Rather than selectively eliminating senescent cells, Rb1 primarily targets senescence-associated dysfunction and restores endometrial homeostasis, highlighting its potential as a senescence-modulating therapeutic strategy for uterine aging.

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Ginsenoside Rb1 may reduce uterine aging by blocking a key cell growth pathway

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