Adipose-derived stem cell exosomes promote neurological recovery after subarachnoid hemorrhage via AMPK/mTOR-mediated TFEB activation.
Liu M., Li S., Wu L., Liu M., Zeng C., Shen J.
Animal Study, published in Neurol Res (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Neurol Res (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40981517
- DOI
- 10.1080/01616412.2025.2559309
Abstract (original English)
Subarachnoid hemorrhage (SAH) is a common neurologically devastating disorder, and existing treatment options remain very limited. Increasing evidence has confirmed the neuroprotective effects of exosomes derived from mesenchymal stem cells (MSC). Our work investigates that adipose-derived stem cell exosomes (ADSC-Exos) exert therapeutic effects against SAH through autophagy-related pathways. An intracerebral perforation method was used to establish a rat SAH model. Then we injected PBS containing 50 µg, 100 µg, or 200 µg of exosomes. Rat neurological deficits and brain water content were assessed. Additionally, brain tissues were collected for Nissl staining, immunofluorescence and Western blot analysis. Furthermore, we utilized oxyhemoglobin (OxyHb) to induce an in vitro SAH model in primary neurons. BML-275 (an AMPK inhibitor) was administered to explore the mechanism of ADSC-Exos-induced autophagy. ADSC-Exos reduced neurological deficits and brain water content in rats with SAH, while also inhibiting neuronal apoptosis. Treatment with ADSC-Exos led to an increase in Beclin1 and LC3 levels. Both Western blot and immunofluorescence analyses revealed that the TFEB nuclear translocation activated after ADSC-Exos treatment. What's more, the level of P-AMPKα/AMPK was increased and P-MTOR/mTOR was decreased. On the other hand, the administration of BML-275 was able to reverse thes
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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