ArticleBasic and clinical neuroscience
The Effects of Hesperidin on BDNF/TrkB Signaling Pathway and Oxidative Stress Parameters in the Cerebral Cortex of the Utero-placental Insufficiency Fetal Rat Model.
Article in Basic and clinical neuroscience. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Neuroactive Phytochemicals as Multi-Target Modulators of Mental Health and Cognitive Function: An Integrative Review.International journal of molecular sciences · 2025Review
- The Effect of Naringin on Cognitive-Behavioral Functions, CREB/BDNF Signaling, Cholinergic Activity, and Neuronal Density in the Hippocampus of an MSG-Induced Obesity Rat Model.Neurotoxicity research · 2025Article
- Hesperidin efficacy of epidural fibrosis in a post laminectomy rat model: an experimental study.Turkish journal of medical sciences · 2025Article
- Harnessing hesperidin for brain metabolism: epigenetic signatures, cellular homeostasis, synaptic function, and neuroprotection in age-related diseases and neurodegenerative diseases.Frontiers in nutrition · 2025Review
- Prangos ferulacea (L.) ameliorates behavioral alterations, hippocampal oxidative stress markers, and apoptotic deficits in a rat model of autism induced by valproic acid.Brain and behavior · 2023Article
- The Impact of Coenzyme Q10 on Cognitive Dysfunction, Antioxidant Defense, Cholinergic Activity, and Hippocampal Neuronal Damage in Monosodium Glutamate-Induced Obesity.Iranian journal of pharmaceutical research : IJPRArticle
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionUteroplacental Insufficiency (UPI) produces critical neurodevelopmental problems affecting the Intrauterine Growth Restricted (IUGR) in offspring. This study aimed to investigate the possible neuroprotective roles of Hesperidin (Hes) on the fetal cerebral cortex of the UPI rat model.
methodsIn this experimental study, 40 pregnant Wistar rats (age: ∼40 days, Mean±SD weight: 180±10 g) were randomly divided into 5 groups (n= 8/group). The study groups included control (normal saline, orally), UPI+NS (uterine vessel ligation+normal saline, orally), UPI+HES25, UPI+HES50, and UPI+HES100 (uterine vessel ligation+25, 50 and 100 mg/kg Hes, orally). After being anesthetized by ketamine and xylazine, UPI was induced by permanent bilateral closure of the uterine vessels on Gestation Day (GD) 18. From GD15, the Hes/NS-treated groups received Hes/normal saline until GD21. On GD21, the uterus, placenta, and fetus were dissected out and weighed. The oxidative stress parameters, including Catalase (CAT) activity, Malondialdehyde (MDA), and Total Antioxidant Capacity (TAC) were measured in the fetal cerebral cortex. The expression of Brain-Derived Neurotrophic Factor (BDNF) and Tropomyosin Receptor Kinase B (TrkB) was assessed by RT qPCR methods. The obtained data were analyzed by Analysis of Variance (ANOVA) and Tukey's post hoc test.
resultsThe present study findings identified a significant difference in the uterine and fetus weight in Hes-treated mothers (P< 0.05). In the fetus, Hes reduced MDA, and increased CAT activity and TAC (P<0.001 in the UPI+Hes100 group, compared to the UPI+NS group). UPI reduced BDNF and TrkB mRNA expression, compared to the control group (P<0.05). Also, Significant increases in BDNF and TrkB mRNA expression were observed after administrating Hes in the fetal cerebral cortex of the UPI rat model, in a dose-dependent manner (P<0.05).
conclusionHes, as a neuroprotective and antioxidant agent, accelerates BDNF-TrkB signaling pathway and suppresses oxidative stress parameters in the cerebral cortex of the UPI rat model.
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