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DOI 10.1002/vms3.70193

Медицинская библиотека · Veterinary medicine and science · 2025

FABP4 Mediates Inflammation to Regulate Endometrial Epithelial Cell Function During Early Gestation in Sheep.

Chen Yan, Liu Chang, Liu Zhijiao, Yu Hengbin, Peng Xiayu, Wang Jing, Hu Guangdong

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

The objective of this experiment was to understand the impact of fatty acid binding protein 4 (FABP4)-mediated inflammation on sheep endometrial epithelial cells (sEECs). To model the hormonal environment of sheep during pregnancy, estradiol (E2), progesterone (P4) and interferon-tau (IFN-τ) were used. The sEECs were then stimulated with different concentrations of lipopolysaccharide (LPS) to determine suitable concentrations for inducing inflammation, while FABP4 expression was inhibited using a FABP4-specific inhibitor. The expression of genes related to inflammation, cell apoptosis, cell proliferation, endometrial tolerance, and embryo development were detected by real-time quantitative PCR and Western blot. The cell proliferation ability was detected by CCK-8, and the cell migration ability was tested by scratch assay. The results showed that LPS-induced inflammation inhibited the expression levels of proliferation genes, migration ability genes and endometrial tolerance-related genes and enhanced the expression levels of apoptosis genes and gestational elongation-related genes and proteins in the sEECs. The use of FABP4 inhibitors reduced LPS-induced inflammation and alleviated the inhibitive effect of LPS on cellular function. The experiments showed that inhibiting the expression of the FABP4 gene reduced LPS-induced inflammation and alleviated the impact of LPS on the viability of sEECs.

Для цитирования: Chen Yan, Liu Chang, Liu Zhijiao, Yu Hengbin, Peng Xiayu, Wang Jing, Hu Guangdong. FABP4 Mediates Inflammation to Regulate Endometrial Epithelial Cell Function During Early Gestation in Sheep.. Veterinary medicine and science. 2025. DOI: 10.1002/vms3.70193.

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