Objective: Although preeclampsia (PE) is one of the most important problems affecting pregnant women, etiologic factors in its development are still unclear. We aimed to investigate the expression levels of cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α) and inducible NO synthase (iNOS) in preeclamptic and healthy control placentas. Patients and methods: Placental tissue samples were obtained after delivery from patients diagnosed with PE and from normal-term pregnants and analyzed for COX-2, TNF-α and iNOS expression by immunohistochemistry. Results: A strong expression of COX-2 was observed in syncytiotrophoblast cells of preeclamptic placentas, which was significantly higher than that of normal placentas (p = 0.005). A mild expression of TNF-α in both normal and preeclamptic syncytiotrophoblasts was seen (p = 0.435). In addition, a strong expression of iNOS in normal syncytiotrophoblasts was found, but the intensity of the iNOS expression was highly reduced in preeclamptic placentas (p = 0.001). No correlation was detected between COX-2, TNF-α and iNOS expression levels. Conclusion: The findings of a decrease of iNOS expression and an increase of COX-2 expression in placenta suggest the existence of functional roles of iNOS and COX-2 in the pathophysiology of PE, probably by contributing to the reduced placental blood flow and increased resistance to flow in the fetomaternal circulation.

Cyclosporine A (CsA) is a drug used in autoimmune disorders and organ transplantations. Omega 3 fatty acids (O-3) and sesame oil (SO) have antioxidant properties. We aimed to investigate and compare the protective effects of O-3 and SO against CsA-induced nephrotoxicity. Seven groups of male Wistar albino rats were included in the study. In group 1 (control), saline was administered, and in group 2, CsA (subcutaneously) was administered. In group 3, CsA+SO (orally; p.o.) was given; in group 4, CsA+O-3 (p.o.) was given; and in group 5, CsA+SO+O-3 was given. In group 6, SO was administered, and in group 7, O-3 was administered. After 15 days of treatment, kidneys were excised. Histopathological evaluation, apoptotic cell count, and renal/hepatic function tests were performed. In group 2, vacuolar degeneration and necrosis of tubular cells as well as hemorrhagic foci were observed; the apoptotic cell number was higher than in the control (P < 0.001). In groups 3, 4, and 5, tubular scores and apoptotic cell count were lower than in group 2 (P < 0.01 and P < 0.001, respectively). In groups 6 and 7, healthy renal histology and a few apoptotic cells were determined. In groups 2, 3, 4, and 5, blood urea nitrogen was higher and albumin was lower than in the control (P < 0.001). Liver enzymes were unchanged. O-3/SO showed similar protective effects against CsA-induced nephrotoxicity, as revealed by a remarkable decrease in histopathological changes and apoptotic cell count. However, impaired renal function tests were not improved with O-3/SO treatment. SO and O-3 can be used as chemoprotectants against CsA.