SVF
Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Hypoxic adipose mesenchymal stem cells derived conditioned medium protects myocardial infarct in rat.

He J., Cai Y., Luo LM., Liu HB.

Animal Study on Cardiovascular Disease, published in Eur Rev Med Pharmacol Sci (2015) — 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
Eur Rev Med Pharmacol Sci (2015)
Country
Italy
Reported sample size
—
Source database
PubMed
PMID
26636529

Abstract (original English)

The aim of this study was to explore the impact of normoxic and hypoxic cell-culture conditions on the expression and secretion of adipose mesenchymal stem cells (ADMSCs)-derived paracrine molecules, and to evaluate the cardioprotective role of hypoxic condition medium (hypoCM) in vivo. Semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) analyses of normoxic and hypoxic ADMSCs and their conditioned medium fractions. Then, the effect of hypoCM on cardiomyocytes proliferation and migration was assessed. Moreover, a rat model of myocardial infarct (MI) was established to test the therapeutic effect of hypoCM in vivo. ADMSCs expressed and secreted significantly higher amounts of vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF) and stromal derived factor-1 (SDF-1 or CXCL12) under hypoxic conditions. Furthermore, compared with the vehicle control, hypoCM significantly enhanced the proliferation and migration of cardiomyocytes. Consistent with the in vitro data, hypoCM decreased the infarct size, apoptosis index and apoptosis related protein in the rat MI model. These findings suggest that ADMSCs promote rat MI via hypoxia-enhanced paracrine.

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
Adipose TissueAnimalsApoptosisCardiotonic AgentsCell HypoxiaCell ProliferationChemokine CXCL12Culture Media, ConditionedHepatocyte Growth FactorHumans
Systemic / IVCardiovascular Disease
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