ArticleTurkish journal of obstetrics and gynecology2024
Evaluation of placental bed uterine in L-NAME-induced early-onset preeclampsia (EO-PE) like the rat model.
Article in Turkish journal of obstetrics and gynecology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Modulation of oxidative stress and angiogenic pathways by natural compounds in experimental preeclampsia: A narrative review focusing on MDA, sFlt-1, and PlGF.Turkish journal of obstetrics and gynecology · 2026Article
- Silibinin Modulates NF-κB Activation and Heat Shock Protein in Preeclampsia-Like Rat Model.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- Ginsenoside Rb1 alleviates endothelial dysfunction and vascular remodeling in preeclampsia via activation of the PI3K-Akt-eNOS pathway.Scientific reports · 2026Article
- Importance of STAT3 signaling in preeclampsia (Review).International journal of molecular medicine · 2025Review
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Authors and funding
4 authors.
Funding
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Abstract
Objective: Preeclampsia (PE) is the leading cause of maternal death worldwide and is associated with long-term morbidity in both mothers and newborns. Animal modeling is considered a functional source for understanding PE pathogenesis, diagnostic standards, and therapeutic approaches. Materials and Methods: This study aimed to demonstrate and evaluate the use of N-nitro-L-arginine methyl ester (L-NAME) in a Wistar rat model under conditions similar to PE. A total of 12 rats were divided into 4 groups, each consisting of 3 members, including the pregnant control group and treatment groups administered low-dose (PE 25 mg/kg L-NAME/day), medium-dose (PE 50 mg/kg L-NAME/day), and high-dose L-NAME (PE 75 mg/kg L-NAME/day) L-NAME from gestational day 4 to 19. Measurements included blood pressure, creatinine, and proteinuria levels, placental histological changes, and placental tissue hypoxia-inducible factor 1-alpha, and plasma endothelial nitric oxide synthase levels. Results: The results showed that intervention with L-NAME at 75 mg/kg body weight/day (PE3) induced PE earlier than that with 50 mg/kg body weight/day L-NAME. Conclusion: The model conditions also support further research into PE pathogenesis.
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