Effects of Stem Cells on Rat Embryo Development in Hypoxy Embryo Culture


Patat D., NİSARİ M., UÇAR S., GÖNEN Z. B., Korkmaz Ş., YAY A. H., ...Daha Fazla

Bratislava Medical Journal, cilt.126, sa.6, ss.881-897, 2025 (SCI-Expanded, Scopus) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 126 Sayı: 6
  • Basım Tarihi: 2025
  • Doi Numarası: 10.1007/s44411-025-00117-5
  • Dergi Adı: Bratislava Medical Journal
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, EMBASE
  • Sayfa Sayıları: ss.881-897
  • Anahtar Kelimeler: Hypoxia, Mesenchymal stem cells, Rat, Stem cell therapy, Whole embryo culture
  • Yozgat Bozok Üniversitesi Adresli: Evet

Özet

Objective: This study aimed to compare the in vitro effects of bone marrow mesenchymal stem cells (BM-MSCs) and adipose tissue mesenchymal stem cells (AT-MSCs) in mitigating intrauterine growth retardation caused by oxidative stress. Materials and Method: 9.5-day-old embryos from Wistar albino pregnant rats were exposed to in vitro hypoxia and treated with BM-MSCs or AT-MSCs in embryo culture. At 11.5 days, embryos and yolk sacs were evaluated morphologically and histologically to assess developmental differences between groups. Results: Hypoxia induced angiogenesis- and neurogenesis-related anomalies. Stem cell treatments (H + BM-MSC, H + AT-MSC) significantly improved embryonic development compared to the hypoxia group (p < 0.05). Although stem cell-treated embryos lagged slightly behind controls under normoxia (p > 0.05), both BM-MSC and AT-MSC applications mitigated hypoxia-related growth defects. Notably, the H + AT-MSC group showed superior development compared to the H + BM-MSC group (p < 0.05), with results closer to the normoxic control group. Conclusion: AT-MSCs demonstrated a more effective improvement in embryonic and yolk sac development compared to BM-MSCs under hypoxic conditions. These findings suggest that AT-MSC therapy could offer a promising approach to treat angiogenetic and neurogenetic disorders caused by oxidative stress.