{"id":368,"title":"Ginsenoside Rb1 alleviates uterine aging via AMPK-mediated mTOR inactivation","title_zh":"人参皂苷Rb1通过AMPK介导的mTOR失活缓解子宫衰老","url":"https://pubmed.ncbi.nlm.nih.gov/42946698","doi":"10.1038/s41392-026-02970-4","pmid":"42946698","journal":"Signal Transduct Target Ther","kind":"paper","lang":"en","published_at":"2026-10-28T00:00:00+00:00","fetched_at":"2026-11-08T03:44:12+00:00","authors":["Zhou P","Wang Y","Cheng M","Deng F","Liu F","Chen X","Ning K","Mo D","Zeng Z","Huang Z","Dong Y","Wang Y","Zhang C","Qiao J","Yu Y","Pan H","Li R"],"primary_topic":"endometrium","topics":[{"slug":"endometrium","score":9.0,"hits":["decidualization","endometrial","endometrium","stromal cell","uterine","uterus"]},{"slug":"repro-aging","score":3.0,"hits":["rapamycin","senescence","senescent"]},{"slug":"art-clinical","score":1.0,"hits":["implantation failure"]},{"slug":"contraception-health","score":1.0,"hits":["reproductive health"]},{"slug":"omics-methods","score":1.0,"hits":["proteomic"]}],"topic_score":9.0,"preference_score":0.0,"preference_labels":[],"llm_score":78.0,"final_score":84.0,"score_dims":{"novelty":72,"rigor":75,"impact":70,"relevance":82,"translation":68},"recommend_reason":"首次将天然产物Rb1与子宫衰老的内膜基质细胞衰老及AMPK-mTOR-NF-κB轴联系起来，机制链条较完整，对内膜衰老与植入失败研究有参考价值；但证据以细胞与小鼠为主，距临床转化尚远。","keywords":["子宫衰老","人参皂苷Rb1","内膜基质细胞","细胞衰老","AMPK-mTOR-NF-κB","内膜蜕膜化"],"selected":1,"story_id":295,"llm_provider":"deepseek","llm_model":"deepseek-flash","llm_effort":"low","source_key":"pubmed-top-journals","source_name":"PubMed · CNS/大子刊/四大医学刊（生殖相关）","source_tier":1,"mention_count":1,"has_interpretation":false,"journal_key":"sttt","journal_tier":"general-top","journal_if":40.8,"is_mock":false,"summary_zh":"本研究探讨人参皂苷Rb1对子宫衰老的作用及机制。作者在衰老的人子宫内膜及小鼠子宫中证实，Rb1可减轻内膜基质细胞（EnSCs）的氧化应激、衰老与凋亡。蛋白组学分析显示Rb1经mTOR相关通路发挥保护作用：Rb1激活AMPK，并由AMPK介导抑制mTOR-NF-κB信号环路，从而改善衰老表型。研究表明Rb1并非选择性清除衰老细胞，而是靶向衰老相关功能障碍、恢复内膜稳态，提示其作为调控衰老的子宫衰老治疗策略的潜力。","summary":"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.","interpretation_basis":null,"fulltext_status":null,"interpretation":null,"fulltext":{"available":false,"status":null,"reason":"尚未抓取全文（未入选、分数未达阈值，或还没跑 fulltext 步骤）","pmcid":null,"license":null,"chars":0,"source":null,"fetched_at":null}}