<p>Preeclampsia, as one of the most common pregnancy-specific diseases, causes high maternal-fetal morbidity and mortality in almost every country. Placental vascular abnormalities in preeclamptic women can cause chronic hypoxia and impaired fetal nutrition, so fetal growth retardation often occurs. EVOO has strong antioxidant effect is assumed to prevent nutritional disorders in the fetus. This study aimed to determine the effect of EVOO on fetal birth weight in a preeclampsia rat model. This research was laboratory research conducted in vivo with a Post Test Only Control Group design which consisted of five groups; negative control group, positive control group (pre-eclampsia rat model), dose 1, 2, and 3 groups that were preeclampsia rats given EVOO in 3 different doses (0.5 mL/day, 1 mL/day and 2 mL/day respectively). Blood pressure and proteinuria measurements were carried out at the 12, 15 and 19 day of pregnancy. After sacrificed, fetal weight was measured immediately using analytical balance. The result of this study showed that there was a significant reduction of fetal weight between negative control and positive control group (p=0.020), meanwhile no significant differences among positive control, dose 1 and dose 2 group (p=0.90 and p=0.142) but statistically significant to dose 3 group (p=0.005). EVOO administration increases fetal weight in doses group by its AA and DHA in Long-Chain Poly Unsaturated Fatty Acids (LCPUFA) within. The optimal dose of EVOO to increase fetal weight is 2 mL/day.</p>
Objective: This study aimed to determine the effect of Extra Virgin Olive Oil (EVOO) on vasodilator enzyme by repairing angiogenic function in rat model of preeclampsia. Materials and methods: This research consisted of five groups; negative control (normal pregnant rats) group, positive control (preeclampsia rat model) group, preeclampsia rat model groups given EVOO in 3 different doses (0.5 ml/day, 1 ml/day, and 2 ml/day, respectively). Blood pressure measurements were carried out on day 12, 15, and 19 of pregnancy. After the rats were sacrificed, the placentas were collected to determine endothelial Nitric Oxide Synthase (eNOS) level of maternal plasma to determine soluble Fms-like Tyrosine Kinase 1 (sFlt-1) and Vascular Endothelial Growth Factor (VEGF) level. Results: There were significant higher sFlt-1 level (p < 0.001), lower VEGF level (p = 0.009), and lower eNOS level (p = 0.034) between negative and positive control groups. After EVOO administration, sFlt-1 level was lower in dose 1 and 2 groups but higher in dose 3 group in accordance with VEGF and eNOS levels that were increasing both in dose 1 and dose 2 groups but decreasing in dose 3. There were significant differences between positive control and dose 1 (p = 0.015) and dose 2 (p = 0.001) in sFlt-1 level. None of all dose groups were statistically different with positive control group in VEGF level (dose 1 p = 0.601; dose 2 p = 0.297; dose 3 p = 0.805). eNOS levels of all dose groups were statistically different from that of the positive control group (dose 1 p = 0.014; dose 2 p = 0.001; dose 3 p = 0.024). Conclusion: Administration of EVOO modulates eNOS as vasodilator enzyme by repairing the angiogenic function indicated by decreased sFlt-1 level and increased VEGF in rat model of preeclampsia.
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