Search

Abstract Objective To investigate the expression of insulin-like growth factor binding protein-3(IGFBP-3) in HELLP syndrome and its possible role in the pathogenesis of this disease. Methods 1) 87 subjects were enrolled, including 29 patients with HELLP syndrome, 29 patients with pre-eclampsia (PE), and 29 healthy gravidae as control. The levels of IGFBP-3, IGF-1, TGF-β1, and VEGF in maternal and umbilical blood of them were detected using ELISA. Correlation analysis was used to observe the correlation between IGFBP-3 and IGF-1/TGF-β1/VEGF in maternal and umbilical blood, as well as that between maternal serum IGFBP-3 and clinical diagnostic indicators of HELLP syndrome. 2) Human hepatic sinusoid endothelial cells (HLSEC) and human umbilical vein endothelial cells (HUVEC) were cultured with different concentrations of IGFBP-3. After 72 h of culture, cell apoptosis and the normal living cells rate were detected and compared. Results 1) In both maternal and umbilical blood of HELLP group, levels of IGFBP-3 and TGF-β1 were higher than control and PE group, IGF-1was lower than control group, VEGF was lower than control and PE group. IGFBP-3 in maternal blood was correlated with IGF-1/TGF-β1/ VEGF, while IGFBP-3 in umbilical blood was linked to IGF-1/TGF-β1. In maternal blood, there was a negative correlation between PLT and IGFBP-3, and a positive correlation between ALT/AST/LDH and IGFBP-3. 2) After cultured with IGFBP-3, the total apoptosis rate of either HLSEC or HUVEC was considerably elevated, while the normal living rate was decreased. Conclusion The expression of IGFBP-3 is elevated in HELLP syndrome, which may subsequently promote cell apoptosis by affecting the expression and function of IGF-1, VEGF, and TGFβ1 in the IGF/PI3K/Akt, TGF-β1/Smad3, and VEGF/eNOS/NO pathways. IGFBP-3 aggravates inflammatory reactions of the vascular endothelium and liver under hypoxia, affects the normal function of cells, and plays a role in the pathogenesis of diseases.

Objective: To study the teratogenicity and traumatic effect of microcystin LR (MCLR) on pregnant SD rats and their fetuses., Methods: Sixty pregnant SD rats were divided into four groups, 16 in each group: three experimental groups in which MCLR was injected into the abdominal cavity at the doses of 4 microgram/kg, 16 microgram/kg, and 62 microgram/kg respectively for 10 days, and control group injected with normal saline. Twenty days after, the pregnant rats were killed. The development, teratosis, and histology of viscera of the fetuses were examined., Results: Deformities were found in the fetuses of the 62 microgram/kg group and 16 microgram/kg group with the teratogenic rate of 11.70 per thousand (2/172) and 6.76 per thousand (1/155). Petechial hemorrhage and severe hydropic degeneration in liver and maldevelopment of glomeruli and renal medulla were found in 62 microgram/kg group. Mild granular degeneration was found in the liver of fetuses in 4 microgram/kg group., Conclusion: MCLR passes through the placental barrier and causes damage in kidney and liver, which may be the basis of high incidence of liver cancer microgram in the fetus phase.