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

Introduction: Uteroplacental 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. M...

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Main Authors: Hamed Abdollahi, Mohammad Amin Edalatmanesh, Ebrahim Hosseini, Mohsen Foroozanfar
Format: Article
Language:English
Published: Iran University of Medical Sciences 2021-07-01
Series:Basic and Clinical Neuroscience
Subjects:
Online Access:http://bcn.iums.ac.ir/article-1-1649-en.html
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author Hamed Abdollahi
Mohammad Amin Edalatmanesh
Ebrahim Hosseini
Mohsen Foroozanfar
author_facet Hamed Abdollahi
Mohammad Amin Edalatmanesh
Ebrahim Hosseini
Mohsen Foroozanfar
author_sort Hamed Abdollahi
collection DOAJ
description Introduction: Uteroplacental 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. Methods: In 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. Results: The 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). Conclusion: Hes, 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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spelling doaj.art-48b8cf712b4b4b429ee0f51c73aec7aa2024-03-03T04:22:14ZengIran University of Medical SciencesBasic and Clinical Neuroscience2008-126X2228-74422021-07-01124511522The Effects of Hesperidin on BDNF/TrkB Signaling Pathway and Oxidative Stress Parameters in the Cerebral Cortex of the Utero-placental Insufficiency Fetal Rat ModelHamed Abdollahi0Mohammad Amin Edalatmanesh1Ebrahim Hosseini2Mohsen Foroozanfar3 Department of Biology, School of Sciences, Shiraz Branch, Islamic Azad University, Shiraz, Iran. Department of Biology, School of Sciences, Shiraz Branch, Islamic Azad University, Shiraz, Iran. Department of Biology, School of Sciences, Shiraz Branch, Islamic Azad University, Shiraz, Iran. Department of Biology, School of Sciences, Marvdasht Branch, Islamic Azad University, Marvdasht, Iran. Introduction: Uteroplacental 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. Methods: In 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. Results: The 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). Conclusion: Hes, 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.http://bcn.iums.ac.ir/article-1-1649-en.htmlhesperidinebrain-derived neurotrophic factoroxidative stressintrauterine growth retardation
spellingShingle Hamed Abdollahi
Mohammad Amin Edalatmanesh
Ebrahim Hosseini
Mohsen Foroozanfar
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
Basic and Clinical Neuroscience
hesperidine
brain-derived neurotrophic factor
oxidative stress
intrauterine growth retardation
title 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
title_full 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
title_fullStr 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
title_full_unstemmed 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
title_short 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
title_sort effects of hesperidin on bdnf trkb signaling pathway and oxidative stress parameters in the cerebral cortex of the utero placental insufficiency fetal rat model
topic hesperidine
brain-derived neurotrophic factor
oxidative stress
intrauterine growth retardation
url http://bcn.iums.ac.ir/article-1-1649-en.html
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