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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Autores principales:	Hamed Abdollahi, Mohammad Amin Edalatmanesh, Ebrahim Hosseini, Mohsen Foroozanfar
Formato:	article
Lenguaje:	EN
Publicado:	Iran University of Medical Sciences 2021
Materias:	hesperidine brain-derived neurotrophic factor oxidative stress intrauterine growth retardation Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
Acceso en línea:	https://doaj.org/article/48b8cf712b4b4b429ee0f51c73aec7aa
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spelling	oai:doaj.org-article:48b8cf712b4b4b429ee0f51c73aec7aa2021-12-05T08:43:44ZThe Effects of Hesperidin on BDNF/TrkB Signaling Pathway and Oxidative Stress Parameters in the Cerebral Cortex of the Utero-placental Insufficiency Fetal Rat Model2008-126X2228-7442https://doaj.org/article/48b8cf712b4b4b429ee0f51c73aec7aa2021-07-01T00:00:00Zhttp://bcn.iums.ac.ir/article-1-1649-en.htmlhttps://doaj.org/toc/2008-126Xhttps://doaj.org/toc/2228-7442Introduction: 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.Hamed AbdollahiMohammad Amin EdalatmaneshEbrahim HosseiniMohsen ForoozanfarIran University of Medical Sciencesarticlehesperidinebrain-derived neurotrophic factoroxidative stressintrauterine growth retardationNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENBasic and Clinical Neuroscience, Vol 12, Iss 4, Pp 511-522 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	hesperidine brain-derived neurotrophic factor oxidative stress intrauterine growth retardation Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
spellingShingle	hesperidine brain-derived neurotrophic factor oxidative stress intrauterine growth retardation Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 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
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.
format	article
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
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_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_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_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
publisher	Iran University of Medical Sciences
publishDate	2021
url	https://doaj.org/article/48b8cf712b4b4b429ee0f51c73aec7aa
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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

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