The Influence of Experimental Chronic Antenatal and Acute Postnatal Hypoxia on the Morphological State of the Liver Stromal Component
Alla B. Zotova
Profil Orcid, Tetiana O. Khramova
Profil Orcid, Ruslan V. Sydorenko
Profil Orcid, Sergiy O. Sherstiuk
Profil Orcid oraz Stanislav I. Panov
Profil Orcid 
Data publikacji: 17 lis 2024
Zakres stron: 438 - 442
Otrzymano: 02 lip 2024
Przyjęty: 02 wrz 2024
DOI: https://doi.org/10.3889/oamjms.2024.11940
Słowa kluczowe
© 2024 Alla B. Zotova et al., published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License.
BACKGROUND
At present, the asymptomatic course of liver pathology in early childhood remains an urgent problem.
AIMS
The objective of the study was the detection of morphological features of the stromal component of the liver of rats, which were at different stages of postnatal ontogenesis and were exposed to chronic antenatal and acute postnatal hypoxia (APH).
MATERIALS AND METHODS
The study material was rat liver tissue of the control group, the APH group, and the chronic antenatal hypoxia (CAH) group.
RESULTS
From day 1 to day 35, CAH leads to an increase and growth of the stromal component in the liver of offsprings due to the development of sclerotic changes caused by activation of collagen formation with a predominance of mature collagen Type I over immature collagen Type III on day 1 and day 14 of the experiment and predominance of collagen Type III over collagen Type I on day 35 of the experiment, increasing the expression of fibronectin. Starting from day 14, APH leads to the development of sclerotic changes in this organ which increase to day 35, less pronounced compared to the detected sclerotic changes in CAH, and manifest in increased expression of fibronectin, activation of collagen formation with a predominance of collagen Type I over collagen Type III on days 14 and 35 of the experiment.
CONCLUSION
CAH from day 1 and APH from day 14 of postnatal life lead to the development of sclerotic changes in the liver of offsprings, which are more pronounced in cases of simulation of CAH and increase with age.