Американское общество гирудотерапии

Traditional Chinese Medicinal Leech Induces Apoptosis and Autophagy in Glioblastoma by SGK1/Caspase-3 and PI3K/AKT/mTOR Pathway

Basic science / preclinical published in CNS Neurosci Ther (2025)

Последнее обновление: June 18, 2026Рецензент: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Research reportФармакология секрета слюнных желёзРазработка лекарственных препаратовWu S et al. · CNS neuroscience & therapeutics, 2025

Abstract

BACKGROUND: Glioblastoma (GBM) represents the most lethal form of high-grade glioma, with current therapeutic options proving largely ineffective. Consequently, there is an urgent need for novel treatment strategies. Recent studies have indicated that the medicinal leech exhibits notable anticancer properties. However, the precise mechanisms underlying these effects remain to be elucidated. METHODS: To investigate the impact of leech drug-containing serum (LDS) on the proliferation, migration, and invasion of GBM cells, a series of assays including CCK-8, ethynyl deoxyuridine (EdU), colony formation, scratch, and transwell assays were employed. Additionally, the apoptosis and autophagy of GBM cells were analyzed using flow cytometry, monodansylcadaverine staining and the immunofluorescence assay. Transcriptomic sequencing of the cells was conducted to identify differentially expressed genes. In vivo, anticancer activity was assessed by developing tumor xenograft models. Western blot analysis was utilized to identify proteins associated with apoptosis and autophagy. RESULTS: Leech drug-containing serum (LDS) significantly inhibited proliferation, migration, and invasion. Furthermore, it induced autophagy and apoptosis in GBM. Differential gene enrichment analysis and pathway validation indicated that LDS exerts anti-GBM effects by modulating the PI3K/AKT pathway. Leech extracts effectively inhibit the growth of GBM in a subcutaneous xenograft tumor model. CONCLUSION: The leech-derived compounds may induce apoptosis and autophagy in GBM by modulating the PI3K/AKT/mTOR signaling pathway, without eliciting significant adverse effects, thereby presenting itself as a promising therapeutic agent.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal Article
Indexed MeSH termsAnimalsGlioblastomaHumansApoptosisAutophagyTOR Serine-Threonine KinasesCell Line, TumorSignal TransductionProto-Oncogene Proteins c-aktMiceProtein Serine-Threonine KinasesLeeches

Резюме

Leech drug-containing serum inhibits proliferation, migration, and invasion of glioblastoma cells while inducing apoptosis and autophagy via SGK1/Caspase-3 and PI3K/AKT/mTOR pathways. Confirmed in subcutaneous xenograft mouse models with no significant adverse effects.

Почему это важно для гирудотерапии

This study investigated the effects of leech drug-containing serum (LDS) on glioblastoma (GBM) using in vitro assays (CCK-8, EdU, colony formation, scratch, transwell, flow cytometry, immunofluorescence) and an in vivo subcutaneous xenograft tumor model. LDS significantly inhibited proliferation, migration, and invasion while inducing autophagy and apoptosis, with transcriptomic and pathway analyses implicating PI3K/AKT/mTOR signaling. The leech extract also effectively inhibited GBM growth in the xenograft model. For ASH's domain, this is relevant as it explores anticancer properties of a medicinal leech preparation, investigating leech-derived compounds as potential therapeutic agents. Caveat: this is preclinical work using cell lines and xenograft models; no human data is presented, and the abstract does not specify the leech species, preparation details, or the xenograft animal species.

Цитирование

Traditional Chinese Medicinal Leech Induces Apoptosis and Autophagy in Glioblastoma by SGK1/Caspase-3 and PI3K/AKT/mTOR Pathway.

Wu S et al. · CNS neuroscience & therapeutics, 2025

Связанный клинический контекст

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Добавлено в библиотеку ASH: May 27, 2026 · Последнее обновление сайта: June 18, 2026

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