Journal
REPRODUCTIVE TOXICOLOGY
Volume 34, Issue 4, Pages 677-685Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.reprotox.2012.09.009
Keywords
Preeclampsia; Inflammation; Trophoblast; Apoptosis; Lipoxin
Categories
Funding
- National Natural Science Foundation of China [81070510]
- Nature Science Foundation of Zhejiang Province, China [Y2101233]
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Preeclampsia (PE) is known to represent an exaggerated maternal inflammatory response to pregnancy. Lipoxin A(4) (LXA(4)), considered as an endogenous stop signal in inflammation, has been extensively studied pre clinically for its inflammatory pro-resolving effects. Thus, in the current study, we tested the effect of BML-111 (synthetic analogue of LXA(4)) on experimental PE rats induced by low-dose endotoxin (LPS) and of LXA(4) on human extravillous trophoblast cell line (TEV-1). In vivo experiment results showed that systolic blood pressure, 24 h-urinary albumin excretion, serum TNF-alpha and IL-8 levels and morphologic damage of placenta and kidney caused by LPS were all effectively alleviated by BML-111. LXA(4) also inhibited LPS-triggered apoptosis, activation of NF-kappa B, TNF-alpha and IL-8 mRNA and protein expression in TEV-1 cells. At the same time, BML-111 protected the cells from LPS-reduced proliferation. The current study demonstrated for the first time that LXA(4) could alleviate the symptoms of PE in endotoxin exposed rats. (C) 2012 Elsevier Inc. All rights reserved.
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