ABSTRACT
Background: Placenta is a central and important focus on the pathogenesis of preeclampsia. Failure of trophoblast cell to the spiral arteries remodeling process due to excessive apoptosis causes uteroplacenter ischaemia and damage of endothelial cells that give rise to clinical manifestations of preeclampsia. Excessive throphoblast apoptosis in preeclampsia mainly occurs through the intrinsic pathway in which expression of Bax protein increases mitocondrial membranes permeability of cytochrom C which further activate the caspase cascade and become involved in the process of cell death. Objective: To compare the expression of Bax protein and throphoblastic apoptosis process between severe preeclampsia/eclampsia and the normotensive pregnancy. Methods: Cross sectional study which consist of 43 severe preeclampsia/eclampsia pregnancies and 38 third trimester normotensive pregnancies, recruited between October 2011 – March 2012. Trophoblastic Bax protein expression is measured by imunohistochemical staining technique and trophoblast apoptosis process is examined by the Tunel assay. Statistical analysis using the independent t test (p<0.05). Results: Bax protein expression was significantly higher in trophoblast cell of severe preeclampsia/eclampsia compared to normotensive pregnancy (1.7 vs 1.4, p=0.00). Bax expression positively correlated (r=0.01) with mean arterial pressure which is increasing of the mean arterial pressure will increase the expression of the Bax protein. There was no significant difference in trophoblastic apoptosis index between severe preeclampsia/eclampsia pregnancy and normotensive pregnancy (23.8 vs 35.5, p= 0.10). Conclusions: Bax protein expression was significantly higher in severe preeclampsia/eclampsia than normotensive pregnancy. There was no significantly difference in trophoblast apoptosis index between severe preeclampsia/eclampsia and normotensive pregnancy. Keywords: trophoblast, severe preeclampsia/eclampsia, Bax protein, apoptosis.
