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Objectives This study evaluated the protective effect of Physalis angulata leaf extract on L-NG-nitroarginine methyl ester (L-NAME)-induced preeclampsia rats. Methods Twenty-five pregnant Wistar rats were randomly divided into five groups. Preeclampsia rats were injected with L-NAME on the 5th to 17th day of gestation (G5-G17), while sham rats were injected with the same vehicle volume. Preeclampsia rats were administered with Physalis angulata leaf methanol extract at 500, 1500, or 2500 mg/kg body weight/day on G1-G17. The systolic blood pressure measurement was performed by the tail-cuff method. Placental VEGFR2 expression was determined by immunohistochemistry. The serum sFlt-1 level was evaluated using ELISA. Serum MDA level, SOD activity, and total nitrite level were measured by colorimetry. Results The L-NAME injection increased systolic blood pressure (1.44-fold), serum sFlt-1 level (1.22-fold), and serum MDA level (2.03-fold). It also decreased placental VEGFR2 expression (1.18-fold), serum SOD activity (2.11-fold), and serum nitrite level (1.25-fold) compared to the Sham group. The extract supplementation prevented the rise in systolic blood pressure and serum sFlt-1 level. It also tended to inhibit the reduction in the placental VEGFR2 expression. It prevented the increase in serum MDA level. It also prevented the decrease in serum SOD activity and nitrite level. Conclusions We concluded that Physalis angulata leaf methanol extract inhibits oxidative stress and an antiangiogenic factor in the rat preeclampsia model. These findings support that the extract has the potential to prevent preeclampsia development. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]