Objective: To evaluate whether estradiol can inhibit and cure the inflammation of experimental preeclampsia in rats.
Methods: Experimental preeclampsia was induced in 14-day-pregnant rats by infusion of endotoxin (1.0 microg/kg). Rats with normal pregnancy were infused with sodium chloride solution. A group of preeclampsia rats was injected with 17beta-estradiol (17beta-E(2), 1 mg.kg(-1).d(-1)). Blood pressure, albuminuria, inflammation associated adhesion molecule CD(49d) and tumor necrosis factor-alpha (TNF-alpha) were assessed.
Results: On pregnant day 19, for normal pregnancy group (group C) the blood pressure was (120.4 +/- 2.0) mm Hg (1 mm Hg = 0.133 kPa), urinary protein (0.47 +/- 0.06) mg/24 hours; for experimental preeclampsia group (group A) blood pressure was (134.2 +/- 2.4) mm Hg, urinary protein (0.79 +/- 0.10) mg/24 hours; for experimental preeclampsia with 17beta-E(2) treatment group (group B) blood pressure was (123.3 +/- 1.7) mm Hg, urinary protein (0.51 +/- 0.08) mg/24 hours. A significant increase of blood pressure and urinary albumin was observed in group A. CD(49d) expression and TNF-alpha concentration were also increased. 17beta-E(2) reduced the expression of CD(49d), concentration of TNF-alpha, blood pressure and albuminuria of experimental preeclampsia. However, the weight of fetuses in 17beta-E(2) treatment group were less than that in other groups.
Conclusion: 17beta-E(2) can improve the symptoms of experimental preeclampsia, but its effects on fetus need to be further studied.