Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

Macrophage autophagy-dependent M2 polarization mediates the protective effect of ADSC-conditioned medium against acute lung injury.

Li J., Yang F., Ren Z., Zhang C., Xing M., Jiao Z.

Animal Study on Chronic Inflammation, Immune Modulation, published in Stem Cell Res Ther (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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
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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
Stem Cell Res Ther (2026)
Country
England
Reported sample size
—
Source database
PubMed
PMID
42050662
PMCID
PMC13270571
DOI
10.1186/s13287-026-04981-y

Abstract (original English)

Background Adipose-derived mesenchymal stem cell conditioned medium (ADSC-CM) has emerged as a promising cell-free therapeutic strategy for acute lung injury (ALI). ADSC-CM's anti-inflammatory effect is closely related to its ability to regulate alveolar macrophage polarization. Furthermore, autophagy in macrophages is considered to be related to the regulation of polarization. However, the specific role and mechanisms by which ADSC-CM coordinates autophagy to guide macrophage polarization are not yet fully clear and urgently require further research. Methods We established an in vivo rat model of LPS-induced ALI to evaluate the ameliorative effects of ADSC-CM. Concurrently, an in vitro model utilizing NR8383 alveolar macrophages was employed to investigate the underlying mechanisms. A comprehensive suite of techniques, including ELISA, flow cytometry, immunohistochemistry, Western blot, and RT-qPCR, was applied for analysis. Result In in vivo experiments, ADSC-CM treatment significantly alleviated LPS-induced pneumonia. In vitro experiments revealed that ADSC-CM enhanced the autophagic flux in NR8383 cells and effectively counteracted the promotion of LPS-driven M1 pro-inflammatory phenotypes, while inducing a shift toward M2 anti-inflammatory phenotypes. This beneficial polarization was proven to be dependent on autophagy, as it was significantly reduced when autophagy was in

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.

How we grade evidence
AnimalsAcute Lung InjuryAutophagyCulture Media, ConditionedRatsMesenchymal Stem CellsLipopolysaccharidesMaleMacrophages, AlveolarRats, Sprague-Dawley

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