Preeclampsia is associated with a deficiency of lipoxin A4 An endogenous anti inflammatory mediator

Capsule:
Lipoxin A4 deficiency may result in preeclampsia because of changes in inflammation, oxidative stress, and 11b-HSD2 expression.

Authors:
Zhangye Xu, M.D., Feng Zhao, M.M., Feng Lin, M.M., Huiqiu Xiang, M.M., Ni Wang, M.M., Duyun Ye, M.M., Yinping Huang, M.M.

Volume 102, Issue 1, Pages 282–290.e4

Abstract:

Objective:
To test whether lipoxin A4 (LXA4) deficiency results in preeclampsia.

Design:
Prospective experimental study.

Setting:
Patient and animal research facilities.

Animal(s):
Sprague-Dawley rats.

Intervention(s):
We measured LXA4 and its biosynthetic enzymes, blocked the LXA4 signaling pathway, treated experimental rats with preeclampsia with LXA4, and detected inflammatory factors, FPR2/ALX, and 11β-HSD2 to systematically test whether lack of LXA4 results in preeclampsia.

Main Outcome Measure(s):
We measured serum levels of LXA4 and inflammatory factors using enzyme-linked immunosorbent assay; detected LXA4 biosynthetic enzymes, inflammatory factors, FPR2/ALX, and 11β-HSD2 mRNA expression using reverse transcriptase–polymerase chain reaction (RT-PCR) and real-time RT-PCR; and localized protein expression using immunohistochemistry.

Result(s):
FPR2/ALX and LXA4 and its biosynthetic enzymes were found to be decreased in women with preeclampsia. Replenishing LXA4 improved the symptoms of lipopolysaccharide-induced rats with preeclampsia, while blocking LXA4 signaling resulted in preeclampsia. LXA4 significantly reduced interleukin-6 (IL-6), tumor necrosis factor-α, and IFN-γ but increased IL-10, LXA4 up-regulated 11β-HSD2.

Conclusion(s):
A deficiency of LXA4 may result in preeclampsia, which might be ascribed to a reduction in inflammation response, oxidative stress, and regulation of 11β-HSD2.

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