STOX1在子痫前期滋养细胞炎症反应中的作用研究#br#

Study on the role of STOX1 in the inflammatory of trophoblast cells in preeclampsia

Objective?To investigate the STOX1 (Storkhead box1) in the inflammatory response of trophoblast cells simulated by human choriocarcinoma cell line JEG3 cells. Methods?The human choriocarcinoma cell line JEG3 cell line was used to mimic trophoblast cells, and a stable transitional cell line model with overexpression/knockdown of STOX1 gene was constructed. 0.05 mmol/L aspirin was added to the experimental and control groups, respectively. Cell migration ability was measured by Transwell, and apoptosis was detected in each group by flow cytometry, and real-time quantitative PCR and protein immunoblotting were used to detect the expression of cell-associated inflammatory, hypoxic and apoptotic factors, biological behavior, and the relative expression of mRNA and protein of molecular biology. Results?Hypoxia-inducible factor α(HIF-1α), endothelial-type nitric oxide synthase (eNOS), and inducible nitric oxide synthase (iNOS), and apoptosis B lymphocytoma-2 (Bcl-2) were significantly reduced in the overexpression STOX1 trophoblast group (P<0.01); meanwhile, inflammatory response-related factor nuclear factor κB (NF-κB), tumor necrosis factor α (TNF-α), interleukin 8 (IL-8) and cysteine protease-3 (Caspase-3) were significantly increased at both gene and protein levels (P<0.05). The expression of hypoxia-inducible genes HIF-1α (P<0.01), eNOS (P<0.05), and iNOS (P<0.001) and anti-apoptotic genes Bcl-2 (P<0.01) was elevated after knockdown of STOX1, while inflammatory responses NF-κB (P<0.05), TNF-α (P<0.01), IL-8 (P<0.01), and Caspase-3 (P>0.05) levels were reduced. Conclusion?STOX1 induces inflammatory response, promotes hypoxia and apoptosis-related gene expression in JEG3 cell line, aspirin may inhibit the effect of STOX1, reduce apoptosis in JEG3 cells, decrease inflammatory response and improve hypoxia in trophoblast cells, and knockdown of STOX1 has synergistic effect with the use of aspirin.