TY - JOUR
T1 - Vitamin D supplementation as a prophylactic therapy in the management of pre-eclampsia
T2 - Focus on VEGF, Ki67, oxidative stress markers in correlation to placental ultra structure
AU - Eissa, Hanan
AU - Abdelsalam, Eman Mohamed
AU - Mokbel, Somaia A.
AU - Elhadedy, Nada H.
AU - Khalil, Rania M.
AU - AbdElfattah, Amany Abd Elfattah Mohamed
AU - Abdel Ghaffar, Dalia M.
AU - El Nashar, Eman Mohamad
AU - Hassan, Alshehri Hanan
AU - Al-Zahrani, Norah Saeed
AU - Aldahhan, Rashid A.
AU - Yassin, Neimat Abd Elhakam
N1 - Publisher Copyright:
© 2025 Elsevier Inc.
PY - 2025/7/1
Y1 - 2025/7/1
N2 - Background: Pre-eclampsia (PE) is a progressive hypertension condition that manifests in the second or third trimester of pregnancy and causes significant proteinuria. A lack of vitamin D (Vit. D) is linked to different pregnancy problems, including impaired placental development. Vitamin D has been shown to enhance fetal growth and lower the incidence of PE. Aim of the work: To better understand the pathophysiological mechanisms behind the PE disease and the therapeutic approaches used to manage it, this study examines the role of Vit. D in placental ischemia and its regulatory effects in Nitro L-arginine Methyl Ester (L-NAME) animal model of PE. Methods: Fifty female rats in the estrus stage were mated with 30 male rats. Thirty female rats were pregnant and divided into three equal groups: control, Preeclampsia group (PE); using L-NAME for induction of PE, and Vit. D group from 7th day then induction by L-NAME at 10th day till end of pregnancy. Mean arterial Bp, proteinuria, oxidative stress markers, histological structure and immunohistochemical expression of Ki67 and VEGF, Morphometric study, and transmission electron microscopy(TEM) were assessed. The results of the current study suggested that, Vit. D supplementation could lower blood pressure, reduce oxidative stress, and restore angiogenic balance through vascular endothelial growth factor (VEGF) and Ki67. Conclusion: For the first time, we conclude that vitamin D supplementation may not only have direct effects on blood pressure regulation and angiogenic hemostasis but also recover placental function, actually contributing to the prevention or management of PE.
AB - Background: Pre-eclampsia (PE) is a progressive hypertension condition that manifests in the second or third trimester of pregnancy and causes significant proteinuria. A lack of vitamin D (Vit. D) is linked to different pregnancy problems, including impaired placental development. Vitamin D has been shown to enhance fetal growth and lower the incidence of PE. Aim of the work: To better understand the pathophysiological mechanisms behind the PE disease and the therapeutic approaches used to manage it, this study examines the role of Vit. D in placental ischemia and its regulatory effects in Nitro L-arginine Methyl Ester (L-NAME) animal model of PE. Methods: Fifty female rats in the estrus stage were mated with 30 male rats. Thirty female rats were pregnant and divided into three equal groups: control, Preeclampsia group (PE); using L-NAME for induction of PE, and Vit. D group from 7th day then induction by L-NAME at 10th day till end of pregnancy. Mean arterial Bp, proteinuria, oxidative stress markers, histological structure and immunohistochemical expression of Ki67 and VEGF, Morphometric study, and transmission electron microscopy(TEM) were assessed. The results of the current study suggested that, Vit. D supplementation could lower blood pressure, reduce oxidative stress, and restore angiogenic balance through vascular endothelial growth factor (VEGF) and Ki67. Conclusion: For the first time, we conclude that vitamin D supplementation may not only have direct effects on blood pressure regulation and angiogenic hemostasis but also recover placental function, actually contributing to the prevention or management of PE.
KW - Angiogenesis
KW - Oxidative stress
KW - Placental ischemia
KW - Placental ultra structure
KW - Pre-eclampsia
KW - Prophylactic therapy
KW - Vitamin D
UR - https://www.scopus.com/pages/publications/105002661042
U2 - 10.1016/j.lfs.2025.123605
DO - 10.1016/j.lfs.2025.123605
M3 - Article
C2 - 40194761
AN - SCOPUS:105002661042
SN - 0024-3205
VL - 372
JO - Life Sciences
JF - Life Sciences
M1 - 123605
ER -