ArticleJournal of molecular histology2024
Amygdalin inhibits endometrial stromal cell proliferation, migration, and invasion in endometriosis mice via inhibiting Wnt/β-catenin signaling.
Article in Journal of molecular histology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Buyang Huanwu Decoction Alleviates Bleomycin-Induced Pulmonary Fibrosis via Wnt/β-catenin and TGF-β1/Smad Pathways.Chemistry & biodiversity · 2026Article
- Mechanisms of Luoshi Neiyi prescription (LSNYP) in endometriosis: a network pharmacology and experimental study.Hereditas · 2026Article
- Molecular mechanisms underlying the inhibition of cell migration and invasion in endometriosis: Advances in pharmacological research (Review).Biomedical reports · 2025Review
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Authors and funding
4 authors.
Funding
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Abstract
To explore the impact of amygdalin on the proliferation, migration, and invasion of human endometrial stromal cells (HESCs) and the possible underlying mechanism. HESCs were incubated with 50, 100, and 200 µg/mL of amygdalin. The malignant activities of HESCs were analyzed by functional experiments. The activation of the Wnt/β-catenin signaling was tested using TOP/FOPFlash. The mRNA expressions of genes were validated by qRT-PCR. The endometriosis (EMS) mouse model was induced and the impact of amygdalin on the growth of ectopic endometrial lesions were assessed. It was observed that amygdalin markedly lessened the malignant activities of HESCs in a dose-dependent way (p < 0.05). Amygdalin dose-dependently declined the activation of TOPFlash and mRNA levels of β-catenin, cyclinD1 and c-Myc in HESCs (p < 0.05). Additionally, the increasing dose of amygdalin progressively inhibited the growth of ectopic endometrial lesions in EMS mouse model (p < 0.05). We reached a conclusion that amygdalin could inhibit the malignant activities of HESCs and alleviate EMS, which was related to Wnt/β-catenin signaling activation.
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Registered trials
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