Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMed

p38 MAPK signaling is a key mediator for low-intensity pulsed ultrasound (LIPUS) in cultured human omental adipose-derived mesenchymal stem cells.

Wang Y., Jiang L., Xu T., Su Z., Guo X., Tu J.

Laboratory Study, published in Am J Transl Res (2019) — 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
Laboratory Study
Journal
Am J Transl Res (2019)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
30787998
PMCID
PMC6357340
Citations
9

Abstract (original English)

Visceral obesity is an independent risk factor for cardiovascular disorders and lacks effective, non-drug based clinical therapy. The use of low-intensity pulsed ultrasound (LIPUS) to treat chronic pain and bone fracture is well-known, but its application for visceral obesity treatment has not been studied. Here, we evaluated the therapeutic potential of LIPUS by studying its effects, at varying doses, on human omental adipose-derived mesenchymal stem cells (hAMSCs). LIPUS stimulation was applied for 1 min at intensities between 70 and 210 mW/cm 2 . Cell viability was measured using the Cell Counting Kit-8 assay. Cell apoptosis was quantified by flow cytometry and immunoblotting of apoptosis marker proteins. We found that a high dose of LIPUS (210 mW/cm 2 ) promoted apoptosis in hAMSCs, while a low dose (70 mW/cm 2 ) increased hAMSC viability. Phosphorylation of p38, a mitogen-activated protein kinase (MAPK), increased with high dose LIPUS treatment, but markedly decreased with a low dose. Inhibition of p38 phosphorylation by SB203580, an inhibitor of p38 MAPK activity, rescued the apoptotic effects of high dose LIPUS. Our results showed the dose-dependent, opposing effects of LIPUS on hAMSCs and suggested that p38 plays a key role in mediating the effects of LIPUS on hAMSCs.

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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