Background: preeclampsia (PE) is a pregnancy related complication defined as a disease that begins in the placenta and ends at the maternal endothelium. It is a multi-stage disease that starts by utero-placental insufficiency and leads to generalized maternal endothelial dysfunction.Lipocalin2 (LCN2) is a 25kDasecretory glycoprotein implicated in many functions such as apoptosis and innate immunity. Also, it has been recognized to have potential effects in obesity, inflammation and insulin resistance in mice and humans. Many controversial studies about the changes in the plasma LCN2 levels in PE are reported.
Aim: The current study was designed to perform an animal model of experimental PE in a trial to demonstrate the possible relationship between PE and the circulating LCN2 levels.
Design: forty eight healthy adult female albino rats and eight adult male albino rats were used. The male rats were used for induction of pregnancy. The adult female rats (n=48) were divided into four equal groups: group I (control non-pregnant group), group II (non-pregnant treated with L-NAME), group III (normal pregnant group) and group IV (pregnant treated with L-NAME to induce a model of experimental PE). In all groups, body weight, body mass index (BMI), blood pressure, circulating levels of urea, creatinine, triglycerides (TGs), IL-6, endothelin-1(ET-1), vitamin D (VD), LCN2 and D-dimers in addition to total urinary proteins are measured. Histopathological examination of placental sections was done in group III and group IV.
Results: The results of the present study revealed a significant increase in the body weight, BMI, MAP, total urinary proteins, circulating levels of urea, creatinine, TGs, IL-6, ET-1, LCN2 and D-dimers in both group II and IV. In addition to a significant decrease in VD in the same two groups. In group III, there was a significant increase in body weight, BMI, total urinary proteins and circulating levels of TGS, D-dimers and LCN2. There was a significant decrease in VD and MAP. Moreover, there was a positive significant correlation between LCN2 and all measured parameters except VD in group IV together with a positive significant correlation between LCN2 and MAP, IL-6, ET-1and D-dimers in group II.The results in group IV are supported by the histopathological examination results.
Conclusion: L-NAME can be used for induction of experimental PE and plasma levels of LCN2 can be used as an indicator for the renal complications and coagulopathies in PE. Further studies are needed to ascertain this association.