Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Adipose stem cells' antagonism in glycosylation of D-galactose-induced skin aging of nude mice and its skin recovery function.

Wang H., Wei S., Xue X., You Y., Ma Q.

Animal Study on Skin Aging, published in Int J Immunopathol Pharmacol (2016) — 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
Read the A–D evidence level guide

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
Int J Immunopathol Pharmacol (2016)
Country
England
Reported sample size
—
Source database
PubMed
PMID
26916459
PMCID
PMC5806762
DOI
10.1177/0394632016634348
Citations
14

Abstract (original English)

This study aims to discuss adipose stem cells' (ASCs) antagonism in glycosylation of D-galactose-induced skin aging of nude mice and its skin recovery function; the study also aims to explore a new mechanism of anti-aging to provide clinical anti-aging therapy with new thoughts and methods. We selected 40 healthy specific pathogen-free (SPF) nude mice and divided them randomly into four groups which were: blank control group; D-galactose + phosphate buffer saline (PBS) group; D-galactose + ASCs treatment group; and D-galactose + aminoguanidine (AG) group. Results showed that the superoxide dismutase (SOD) level of mice in the D-galactose-induced model group (87.15 ± 4.95 U/g) decreased significantly compared with that of control group (146.21 ± 4.76 U/g), while malonaldehyde (MDA) level of mice in D-galactose induced model group (11.12 ± 2.08 nmol/mg) increased significantly compared with that of control group (5.46 ± 2.05 nmol/mg) (P <0.05); thus D-galactose induced sub-acutely aging mice models were duplicated successfully. Results also indicated that transplantation of ASCs could reverse expression of aging-related biomarkers such as MDA, SOD, and advanced glycosylation end products (AGEs); hematoxylin and eosin (HE) staining showed that thickness of the dermis layer as well as the collagen content of mice in the D-galactose-induced model group increased significantly after

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
AdipocytesAdipose TissueAnimalsCell DifferentiationCollagenGalactoseGlycosylationMalondialdehydeMiceMice, Inbred C57BL

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