Abstract

Cyclophilin A regulates the biological behavior of placental trophoblast cells in severe preeclampsia by regulating oxygen inducible factor (hypoxia-inducible factor-1 alpha) signal pathway. JEG3 cell line was selected and randomly divided into control group (minimum essential medium 1 l containing 10 % fetal bovine serum) (group A), low dose group (cyclophilin A protein concentration was 1 pg/ml) (group B) and high dose group (cyclophilin A protein concentration was 3 pg/ml) (group C). The apoptosis of JEG3 cells was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling method, the expression of tumor necrosis factor-alpha, interleukin-6 and interleukin-1 beta messenger ribonucleic acid in JEG3 cells was detected by quantitative read-time polymerase chain reaction method, and the expression of cleaved caspase-3, caspase-3, cleaved poly (ADP-ribose) polymerase 1, poly (ADP-ribose) polymerase 1, p53 and hypoxia-inducible factor-1 alpha protein was detected by Western bolting. Quantitative polymerase chain reaction assay showed that the expression levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-1 beta in group B and group C were raised than those in group A, and the expression levels of tumor necrosis factor-alpha, interleukin-6 and interleukin-1 beta increased with the increase of cyclophilin A concentration. Western blotting detection showed that the cleaved caspase-3 expression level of JEG3 cells in group B and C was raised than that in group A, and increased with the increase of concentration, while the expression of cleaved poly (ADP-ribose) polymerase 1 in group C was raised than that in group A. The levels of hypoxia-inducible factor-1 alpha in JEG3 cells were higher in both the group B and C compared to the group A, and they further increased with the rise in concentration. Cyclophilin A can promote inflammation by increasing the expression of tumor necrosis factor-alpha, interleukin-6 and interleukin-1 beta in trophoblasts, and accelerate the apoptosis of trophoblasts by activating caspase-3 pathway, which is an important pathogenic factor of preeclampsia. This mechanism may be related to the regulation of hypoxia-inducible factor-1 alpha signal pathway.