Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Adipose tissue- derived mesenchymal stem cells versus puerarin for ameliorating nicotine- induced pancreatic fibrosis in rats.

Ibrahim HF., Thabet EH., Assem S., Mady B., Elatrebi S., Ali MA.

Animal Study on Systemic / IV, published in Tissue Cell (2025) — 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
Tissue Cell (2025)
Country
Scotland
Reported sample size
—
Source database
PubMed
PMID
41468878
DOI
10.1016/j.tice.2025.103295

Abstract (original English)

Chronic pancreatitis is a critical health problem that is usually complicated by pancreatic fibrosis and diabetes mellitus. Nicotine is a considerable etiological risk factor for this condition. Our research was constructed to explore and compare between the possible therapeutic roles of adipose tissue- derived mesenchymal stem cells (AT- MSCs) and puerarin (Pue) in improving nicotine-induced pancreatic fibrosis. Rats were randomly distributed into: group I; control rats and group II; nicotine- treated rats. Group II was further divided into; model, AT-MSCs- treated, Pue-treated and withdrawal groups. Weight gain study and intraperitoneal glucose tolerance tests were assessed. Pancreatic tissue was processed for measurement of amylase, lipase, interleukin- 6, malondialdehyde and superoxide dismutase. Furthermore, quantitative RT-PCR of caspase-3, transforming growth factor-beta1 (TGF- β1), alpha-smooth muscle actin (α-SMA) and collagen I, was performed. Histopathological, immunohistochemical and ultra-structural examinations were conducted as well. We found that administration of AT- MSCs and Pue helped to increase insulin secretion and suppress inflammatory oxidative stress parameters. In addition, apoptosis and fibrosis were receded through declining of caspase-3 and elements of TGF-β1/α-SMA/collagen I fibrotic pathway. The pancreatic architecture was restored to a great exte

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
AnimalsFibrosisRatsMesenchymal Stem CellsNicotineMesenchymal Stem Cell TransplantationPancreasIsoflavonesAdipose TissueMale

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