Expression And Significance Of Advanced Glycation End Products In Placental, Serum And Umbilical Cord Blood In Pre-eclampsia And Trophoblast Mitochondrial Oxidative Stress Damage

ObjectiveTo study the function of free fatty acid (FFA) in maternal serum and advancedglycation end products (AGEs) in maternal serum, umbilical cord blood and in theplacental of women with pre-eclampsia (PE).MethodsA total of60women with PE and60normal pregnant women as controlparticipated in this study. Patients with PE were divided into early-onset group(presented at<34weeks of gestation, n=30) and late-onset group(presented at≥34weeks of gestation, n=30), with30normal pregnant women as early controlgroup(<34weeks of gestation) and30as late control group(≥34weeks of gestation).Competitive enzyme-linked immunosorbent assay (ELISA) was used to measure theAGEs in maternal serum and umbilical cord blood. Western blotting was performed toanalyze AGEs in the placenta. Improved copper agent colorimetry was performed tomeasure FFA in maternal serum. t-test, one-way ANOVA and pearson correlationanalysis were used for analysis.Results1. In the early-onset and late-onset pre-eclampsia groups, the levels of totalcholesterol(TC), triglyeride(TG), low density lipoprotein cholesterol(LDL),apolipoproteinB(ApoB) were higher than that of their controls, while high densitylipoprotein cholesterol(HDL) and apolipoprotein AI(ApoAl) were lower than that of their controls (P<0.05).2. The mean level of AGEs in maternal serum in the early-onset and late-onsetpre-eclampsia groups was significantly higher than in the control groups.3. The mean concentration of umbilical cord blood AGEs was significantlyhigher in early-onset and late-onset pre-eclampsia groups when compared with thecontrol groups.4. Western blotting revealed that the level of placental AGEs in the early-onsetand late-onset pre-eclampsia groups was significantly higher than in normal placenta.5. Improved copper agent colorimetry analyses showed that the level of serumFFA in the early-onset and late-onset pre-eclampsia groups was higher than in healthypregnant women.6. Maternal serum FFA in early-onset and late-onset pre-eclampsia groupscorrelated positively with serum TG(r=0.778and r=0.610, P<0.05). Maternal serumAGEs in early-onset and late-onset pre-eclampsia groups correlated positively withserum TG(r=0.525and r=0.441, P<0.05). Maternal serum FFA in early-onset andlate-onset pre-eclampsia groups correlated positively with serum AGEs (r=0.764andr=0.774, P<0.05).Conclusions1. Blood lipid metabolic abnormalities in pre-eclampsia.2. AGEs and FFA, which are upregulated in pre-eclampsia.3. AGEs and FFA are likely to be involved in pre-eclampsia through somecommon mechanism. ObjectiveTo investigate free fatty acid analog pre-eclampsia serum, AGEs and CoQ10onthe influence of oxidative stress damage of trophoblast cell mitochondria.MethodsHuman trophoblast cell from early pregnancy women (6～8weeks) werecultured by enzyme-digestion method. when trophoblast cell reached approximately70%～80%after passages, incubated with normal, pre-eclampsia serum and free fattyacid simulation the pre-eclampsia serum concentration for24hours. The fluorescentdye assay was applied to measure the mitochondrial membrane potential; fluorescencemicroscopy and multiskan was used to measure the activity of mitochondrialpermeability transition pore; the expression of mitochondrial DNA was detected byReal-time fluorescence quantitative RT-PCR.Detected the the levels of mitochondrial oxidative stress damage after culturedcells with pre-eclampsia maternal serum for24hours. After that, one group continuedto culture cells with pre-eclampsia maternal serum, another group plused AGEs600mg/L and incubated for16hours before detecting the levels of mitochondrialoxidative stress damage.Cultured cells for24hours with pre-eclampsia maternal serum. Then detectedthe levels of mitochondrial oxidative stress damage. Cultured cells for16hours withCoQ100.5ug, then detected the levels of mitochondrial oxidative stress damage.Results1. The levels of mitochondrial oxidative stress damage in pre-ecampsia groupwere higher than normal pregnant group, the differences were statistically significant(P<0.05).2. The levels of mitochondrial oxidative stress damage in free fatty acid groupwere higher than normal pregnant group, the differences were statistically significant(P<0.05). 3. There was no statistically significant (P>0.05) between free fatty acid groupand pre-ecampsia group about the levels of mitochondrial oxidative stress damage.4. The levels of mitochondrial oxidative stress damage in AGEs group werehigher than concurrent control group, the differences were statistically significant(P<0.05).5. The levels of mitochondrial oxidative stress damage in AGEs group werehigher than before not added group, the differences were statistically significant(P<0.05).6. The levels of mitochondrial oxidative stress damage in CoQ10group werelower than before not added group, the differences were statistically significant(P<0.05).Conclusions1. The pre-eclampsia serum can lead to trophoblast cell mitochondrial oxidativestress damage, may be caused by the free fatty acid in the serum.2. AGEs can cause trophoblast cell mitochondrial oxidative stress damage. AGEsinvolved in the pathogenesis of pre-eclampsia possible through the enhancement ofmitochondrial oxidative stress damage.3. CoQ10had a protective effect on mitochondrial oxidative stress damage.