Adipose-derived Mesenchymal Stem Cells-Derived Exosomes Alleviate LPS-Induced Hepatocyte Injury in Sepsis by Inhibiting the JAK2/STAT3 Signaling Pathway.
Yi X., Lin T., Shen X., Liu B., Mao H., Zheng M.
Laboratory Study, published in Tohoku J Exp Med (2026) — 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
- Laboratory Study
- Journal
- Tohoku J Exp Med (2026)
- Country
- Japan
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41638672
- DOI
- 10.1620/tjem.2025.J174
Abstract (original English)
The severity of sepsis-induced hepatic injury severely impacts disease progression and prognosis. Hence, this study investigates the role of adipose-derived mesenchymal stem cells (ADSCs)-derived exosomes (ADSCs-exo) in mitigating hepatic injury during sepsis. An in vitro model of sepsis-induced hepatic injury was established by stimulating HepG2 cells with lipopolysaccharide (LPS). ADSCs were either co-cultured with LPS-injured HepG2 cells or used to isolate exosomes for subsequent treatment. The characteristics of ADSCs-derived exosomes were identified using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blot. ADSCs-exo uptake by hepatocytes was assessed via PKH67 labeling. Cell viability, apoptosis, and lactate dehydrogenase (LDH) release were evaluated using Cell Counting Kit-8, flow cytometry, and commercial assays, respectively. The involvement of the janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway was further investigated. Both ADSCs and ADSCs-exo notably attenuated LPS-induced hepatocyte injury, as evidenced by lowered LDH release, enhanced cell viability, and suppressed apoptosis. ADSCs-exo were internalized by HepG2 cells. Treatment with ADSCs-exo led to a notable downregulation of phosphorylated JAK2 and STAT3. Moreover, pharmacological activation of the JAK2/STAT3 pathway p
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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