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Journal : Universa Medicina

Recombinant vascular endothelial growth factor 121 decreases vascular cell adhesion molecule-1 in murine pre-eclampsia model placenta Sulistyowati, Sri; Sondakh, John Arianto; Yuliantara, Eric Edwin; Respati, Supriyadi Hari; Soetrisno, Soetrisno
Universa Medicina Vol 35, No 3 (2016)
Publisher : Faculty of Medicine, Trisakti University

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2016.v35.192-198

Abstract

BackgroundPreeclampsia is one of the major contributors to maternal and fetal morbidity and mortality. Imbalance of soluble Fms-like tyrosine kinase (sFlt-1) as anti-angiogenic factor and vascular endothelial growth factor (VEGF) as pro-angiogenic factor plays a role in the pathogenesis of preeclampsia. Endothelial dysfunction in preeclampsia causes vascular cell adhesion molecule-1 (VCAM-1) to be expressed on its surface. This study aims to evaluate the effect of recombinant VEGF-121 on VCAM-1 expression in the placenta of a murine preeclampsia model. Methods An experimental analytical study conducted from February until March 2016 in the Biomedical Laboratory, Faculty of Veterinary Medicine, Airlangga University. The study sample consisted of 30 pregnant mice, divided into three groups, i.e. 10 normal pregnant mice, 10 mice with preeclampsia model and 10 mice with preeclampsia model and recombinant VEGF-121 therapy. All animals were subjected to immunohistochemical examination of VCAM-1 expression in their placentas. The results were assessed semiquantitatively according to a modified Remmele method. Data analysis was done using one-way ANOVA and Tukey’s multiple comparisons method. ResultsMean VCAM-1 expression in normal (0.97 ± 0.54%) murine placentas, compared with placentas (2.94 ± 0.96%) of murine preeclampsia models (p=0.000), while mean VCAM-1 expression in placentas of murine preeclampsia models with VEGF intervention was 2.14 ± 0.68% (p=0.030).Conclusion Recombinant VEGF-121 can reduce VCAM-1 expression in placentas of murine preeclampsia models. The present study has shown the potential benefits of VEGF therapy, justifying serious consideration of this therapeutic approach for use in women with preeclampsia.
L-arginine improves uterine spiral arterial wall thickness in mouse models of preeclampsia Soetrisno, Soetrisno; Sulistyowati, Sri; Wibowo, Anwar Sandi
Universa Medicina Vol 36, No 2 (2017)
Publisher : Faculty of Medicine, Trisakti University

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2017.v36.131-137

Abstract

BackgroundPreeclampsia is a major cause of maternal and fetal morbidity and mortality. The imbalance of anti-angiogenic and angiogenic factors plays a role in endothelial dysfunction in preeclampsia. L-arginine is expected to improve the process of spiral artery remodeling. This study aims to examine the use of L-arginine to repair endothelial damage by measuring the thickness of uterine spiral arteries in mouse (Mus musculus) models of preeclampsia.MethodsThe researchers carried out an experimental study using 30 sixteen-day old pregnant Swiss mice (in good health, weighing 20-25 grams), which were randomly divided into 3 groups (each consisting of 10 mice). The groups were as follows: 1) normal pregnancy K(-); 2) preeclampsia model K(+); and 3) preeclampsia model receiving L-arginine (P). The authors performed histopathological examination of the mouse placenta, which had been dissected, embedded in paraffin wax and subsequently stained with hematoxylin and eosin (HE). The results were analyzed in SPSS v. 21 for Windows using Anova with Tukey.ResultsThe mean thickness of spiral arteries in group K(-) was 53.95 + 26.96 mm, in K(+) 96.50 + 16.66 mm, and in P 62.79 + 8.04 mm. Statistically, there were significant differences between groups K(-) and K(+) (p=0.001) and between K(+) and P (p=0.000), but non-significant differences between K(-) and P (p=1.000).ConclusionsThe treatment with L-arginine proved to be effective in repairing endothelial damage by reducing intimal hyperplasia and atherosis and, in turn, the thickness of uterine spiral arteries in mouse models of preeclampsia.