Preeclampsia is associated with a deficiency of lipoxin A4, an endogenous anti-inflammatory mediator  

Oleh:

Zhangye, Xu ; Feng, Zhao ; Feng, Lin ; Huiqiu, Xiang ; Ni, Wang

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 102 no. 01 (Jul. 2014), page 282–290.
Topik: Preeclampsia; lipoxin A4; inflammation; 11ß-HSD1; 11ß-HSD2

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2014.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

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 11ß-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 11ß-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-a, and IFN-? but increased IL-10, LXA4 up-regulated 11ß-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 11ß-HSD2.

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