Protective Effects of Adipose Mesenchymal Stem Cell Secretome On Oxidative Stress-Induced Bisphenol-A in Isolated Rat Testes Mitochondria and Sperm Quality.
Soleimani MZ., Khorsandi L., Asadi-Fard Y., Rezaei-Tazangi F., Ashtari A.
Animal Study, published in JBRA Assist Reprod (2025) — summary generated from the PubMed abstract.
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
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
- JBRA Assist Reprod (2025)
- Country
- Brazil
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39688440
- DOI
- 10.5935/1518-0557.20240089
Abstract (original English)
This study aimed to explore the potential protective effects of adipose-derived mesenchymal stem cell secretome (ASE) on oxidative stress triggered by Bisphenol-A (BisA) exposure in testicular mitochondria and sperm quality of rats. Testicular tissue mitochondria and sperms were exposed to BisA (8 μM) and ASE (50 or 100 μg). ∆Ψm (mitochondrial membrane potential), reactive oxygen species (ROS) levels, antioxidant biomarkers, and sperm parameters were measured. BisA elevated biomarkers of oxidative stress in mitochondria, while the levels of antioxidant activity and ∆Ψm decreased significantly. BisA harmed the morphology, survival rate, and mobility of the spermatozoids. ASE lowered malondialdehyde contents and ROS generation in the mitochondria, increased ∆Ψm, and reversed sperm quality. These data indicated that ASE effectively reduced BisA-induced damage to mitochondria and enhanced sperm quality by averting oxidative stress.
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 evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.