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Administration of Akebia Saponin D Improved Blood Lipid Levels and Pregnancy Outcomes in Mice with Gestational Diabetes Mellitus

BACKGROUND: Gestational diabetes mellitus (GDM) is a prevalent and severe metabolic disease in pregnant women that is characterized by a high incidence. Placental oxidative stress and inflammation are recognized as the primary contributors to GDM pathogenesis. The repressive effect of akebia saponin...

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Detalles Bibliográficos
Autores principales: Chen, Wei, Shi, Juan, Zhang, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Galenos Publishing 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10613745/
https://www.ncbi.nlm.nih.gov/pubmed/37815409
http://dx.doi.org/10.4274/balkanmedj.galenos.2023.2023-6-82
Descripción
Sumario:BACKGROUND: Gestational diabetes mellitus (GDM) is a prevalent and severe metabolic disease in pregnant women that is characterized by a high incidence. Placental oxidative stress and inflammation are recognized as the primary contributors to GDM pathogenesis. The repressive effect of akebia saponin D (ASD) on oxidative stress and inflammation has been demonstrated in various diseases. AIMS: To investigate the impact of ASD on GDM. STUDY DESIGN: Animal experimental study. METHODS: GDM mice were intraperitoneally treated with ASD. The effect of ASD on GDM symptoms, blood lipid levels, pancreatic tissue damage, gestational outcomes, oxidative stress, and inflammation was assessed via intraperitoneal glucose and insulin tolerance tests, serum glucose and insulin level determination, lipid biochemistry analysis, pathological staining, oxidative stress evaluation, western blot analysis, and enzyme-linked immunosorbent assay. RESULTS: ASD reduced the GDM-induced increase in body weight and blood glucose levels while restoring the decreased insulin levels associated with GDM. In addition, ASD improved the serum lipid parameters, pancreatic tissue damage, and gestational outcomes in GDM mice. Furthermore, ASD reversed the decreased levels of superoxide dismutase and glutathione while reducing the elevated concentrations of malondialdehyde and myeloperoxidase in GDM mice. In addition, ASD rescued the relative protein expression of nuclear factor-E2-related factor 2 and heme oxygenase-1 in the placenta of GDM mice. Additionally, ASD counteracted the increase in tumor necrosis factor-α, interleukin (IL)-6, and IL-1β levels in the sera and placenta of GDM mice. CONCLUSION: ASD suppressed oxidative stress and inflammation to effectively relieve symptoms and gestational outcomes of the GDM mice.