Preeclampsia is associated with a deficiency of lipoxin A4 An endogenous anti inflammatory mediator
Lipoxin A4 deficiency may result in preeclampsia because of changes in inflammation, oxidative stress, and 11b-HSD2 expression.
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
To test whether lipoxin A4 (LXA4) deficiency results in preeclampsia.
Prospective experimental study.
Patient and animal research facilities.
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.
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.
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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