Melatonin influences on steroidoigenic gene expression in the ovary of pinealectomized rats

Because Cyp17a1 expression level was increased in the theca interna and interstitial cells in pinealectomized rats receiving vehicle, melatonin may influence CYP17A1 expression and steroidogenesis in the ovaries.


Carla C. Maganhin, M.D., Ph.D. Ricardo S. Simões, M.D., Ph.D., Luiz Fernando P. Fuchs, M.D., Ph.D., Gisela Rodrigues S. Sasso, M.D., Ph.D., Manuel J. Simões, M.D., Ph.D., Edmund C. Baracat, MD., Ph.D., José Maria Soares Jr., M.D., Ph.D.

Volume 102, Issue 1, Pages 291–298



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


Prospective experimental study.


Patient and animal research facilities.


Sprague-Dawley rats.


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.

Read the full text at:

Please sign in or register for FREE

Your Fertility and Sterility Dialog login information is not the same as your ASRM or EES credentials. Users must create a separate account to comment or interact on the Dialog.