Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Repair effect of adipose-derived mesenchymal stem cell-conditioned medium on cyclophosphamide-induced ovarian injury in mice.

Liu S., Liu W., Liu Y., Luo D., Feng J., Hou L.

Animal Study on Hair & Scalp, Systemic / IV, published in Reprod Toxicol (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
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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
Reprod Toxicol (2025)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
40254105
DOI
10.1016/j.reprotox.2025.108923

Abstract (original English)

The chemotherapeutic drug cyclophosphamide (CTX) may damage the ovarian tissue of females and induce premature ovarian insufficiency (POI). This study aimed to investigate the therapeutic effect of adipose-derived mesenchymal stem cell-conditioned medium (ADSC-CM) on CTX-induced POI mice, and to provide new support for the clinical use of cell-free therapy for POI. Female mice were treated with CTX intraperitoneal injection for 2 weeks, followed by ADSCs or ADSC-CM by intravenous injection for 2 weeks. At the end of the experiment, various parameters were assessed, including ovarian interstitial fibrosis, cell proliferation, follicular count, the levels of follicle-stimulating hormone (FSH) and estradiol (E 2 ), and the expression of gonadal hormone receptor. Additionally, we assessed the levels of oxidative stress, apoptosis, and apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) signaling pathway-related proteins and genes in ovarian tissue. The results showed that ADSCs or ADSC-CM treatment reduced ovarian interstitial fibrosis, promoted the proliferation of cells in the follicles, and increased the number of follicles and ovarian function. In addition, ADSCs and ADSC-CM also reduced the levels of ovarian oxidative stress, decreased the apoptosis of granulosa cells (GCs), and inhibited the activation of ASK1/JNK signaling pathway. In conclusion, our st

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
AnimalsFemaleCyclophosphamideCulture Media, ConditionedMesenchymal Stem CellsPrimary Ovarian InsufficiencyOvaryMiceAdipose TissueApoptosis

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