Format

Send to

Choose Destination
Sci Rep. 2018 Jan 10;8(1):279. doi: 10.1038/s41598-017-18553-x.

Role and mechanism of AT1-AA in the pathogenesis of HELLP syndrome.

Author information

1
Department of Infectious Diseases, Jinshan Hospital, Fudan University, Shanghai, 201508, China. 18930819609@163.com.
2
Department of Obstetrics, The First Hospital, Shanxi Medical University, Taiyuan, Shanxi, 030001, China.
3
Department of Critical Care Medicine, Weifang People's Hospital, Weifang, Shandong, 261041, China.
4
Department of Physiology, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200025, China.
5
Department of Physiology, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200025, China. zhijm@shsmu.edu.cn.

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.

PMID:
29321548
PMCID:
PMC5762787
DOI:
10.1038/s41598-017-18553-x
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center