Abstract
HELLP syndrome remains a leading cause of maternal and neonatal mortality and morbidity worldwide, which symptoms include hemolysis, elevated liver enzymes and low platelet count. The objective of this study was to determine whether HELLP is associated with AT1-AA. The positive rate and titer of AT1-AA in plasma from pregnant women were determined, and the correlation of AT1-AA titer with the grade of HELLP was analyzed. A HELLP rat model established by intravenous injection of AT1-AA. Our experimental results show the AT1-AA titer and positive rate were significantly higher in HELLP group, and AT1-AA titer were positively correlated with the level of TNF-α and ET-1 in plasma and the grade of HELLP syndrome. The results of animal experiments showed that the typical features of HELLP in the pregnant rats after AT1-AA injection. The levels of TNF-α and ET-1 in plasma and liver tissue were significantly increased in AT1-AA-treated rats compared with control rats. The HELLP syndrome induced by AT1-AA was attenuated markedly after administration of losartan. These data support the hypothesis that one the potential pathway that AT1-AA induce damage to capillary endothelial cells and liver during pregnancy is through activation of TNF-α and ET-1.
Highlights
Introduction of the antibody into ratsAll studies were performed in 230 to 250 g timed-pregnant Sprague Dawley (SD) rats
Preeclampsia and HELLP syndrome are idiopathic diseases originating from the placenta during pregnancy, constituting two main causes of maternal death, fetal death and premature birth
Some studies reported that HELLP was the severe form of Preeclampsia, while others argued that some HELLP patients only presented hypertension without proteinura, edema and other characteristic features of preeclampsia
Summary
All studies were performed in 230 to 250 g timed-pregnant Sprague Dawley (SD) rats. After AT1-AA injection, some pregnant rats received losartan (10 mg/kg/day by gavage) for a period of 10 days (Group T, n = 6). Part of the pregnant rats infused with IgGs from the control group served as controls (Group C, n = 6). On GD 19, all rats were placed in metabolic cages for 24-h urine collection. On GD 20, the rats had been anesthetized (sodium pentobarbital 50 mg/kg intraperitoneally), and mean arterial pressure (MAP) was measured by common carotid arterial catheterization as described previously[27]. The biochemical components of HELLP syndrome were measured in plasma and whole blood with respect to hemolysis (LDH and bilirubin), elevated liver enzyme (AST), and platelet levels. All pregnant rats were cesarean section, the numbers of live and dead fetal rats and the body weight of the live rats were record
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