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Volume 10, Issue 2 (Spring 2024)
Caspian J Neurol Sci 2024, 10(2): 93-101 |
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Ethics code: IR.SHAHED.REC.1401.058
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Fathi M, Hassanpourezatti M. Potential Mechanisms Involved in the Anticonvulsant Effect of Recombinant Human VEGF on Maximal Electroshock-induced Seizure. Caspian J Neurol Sci 2024; 10 (2) :93-101
URL: http://cjns.gums.ac.ir/article-1-675-en.html
URL: http://cjns.gums.ac.ir/article-1-675-en.html
1- Department of Biology, Faculty of Basic Sciences, Shahed University, Tehran, Iran.
2- Department of Biology, Faculty of Basic Sciences, Shahed University, Tehran, Iran. , hassanpour@shahed.ac.ir
2- Department of Biology, Faculty of Basic Sciences, Shahed University, Tehran, Iran. , hassanpour@shahed.ac.ir
Abstract: (142 Views)
Background: Vascular endothelial growth factor (VEGF) signaling pathway plays an important role in the pathogenesis of seizure. The oxidant/antioxidant factors and miRNA expression in the brain are differentially regulated in seizure.
Objectives: We aim to investigate the potential mechanism of action for the recombinant human VEGF (rhVEGF) in mice with maximal electroshock (MES)-induced seizure.
Materials & Methods: A total of 40 male mice (weight: 20-25 g) were treated intraperitoneally with normal saline, or rhVEGF (50, 100, and 150 µg/kg, daily for 4 consecutive days). One hour after the last injection, seizures were induced in each animal by MES. The latency for the onset of the first clonus and the duration of hind limb extension (HLE) were recorded. The levels of nitric oxide (NO), total antioxidant capacity (TAC), and micoRNA-142-5p expression were determined in the hippocampus of mice. Blood-brain barrier (BBB) permeability was also estimated by Evans blue dye extravasation method.
Results: The administration of rhVEGF at all doses significantly reduced the HLE duration. However, latency for the seizure onset increased after administration of 50 and 150 μg/kg rhVEGF and decreased after administration of 100 μg/kg rhVEGF. In the brain, the NO level decreased, while TAC level and microRNA-142-5p expression increased by rhVEGF treatment in mice with MES-induced seizure. Pretreatment with rhVEGF at doses of 100 and 150 μg/kg reversed the increase in BBB leakage induced by MES-induced seizures.
Conclusion: The rhVEGF administration can prevent MES-induced seizures by regulating NO, TAC, and miR-142-5 expression levels in the hippocampus and reducing BBB leakage in mice.
Objectives: We aim to investigate the potential mechanism of action for the recombinant human VEGF (rhVEGF) in mice with maximal electroshock (MES)-induced seizure.
Materials & Methods: A total of 40 male mice (weight: 20-25 g) were treated intraperitoneally with normal saline, or rhVEGF (50, 100, and 150 µg/kg, daily for 4 consecutive days). One hour after the last injection, seizures were induced in each animal by MES. The latency for the onset of the first clonus and the duration of hind limb extension (HLE) were recorded. The levels of nitric oxide (NO), total antioxidant capacity (TAC), and micoRNA-142-5p expression were determined in the hippocampus of mice. Blood-brain barrier (BBB) permeability was also estimated by Evans blue dye extravasation method.
Results: The administration of rhVEGF at all doses significantly reduced the HLE duration. However, latency for the seizure onset increased after administration of 50 and 150 μg/kg rhVEGF and decreased after administration of 100 μg/kg rhVEGF. In the brain, the NO level decreased, while TAC level and microRNA-142-5p expression increased by rhVEGF treatment in mice with MES-induced seizure. Pretreatment with rhVEGF at doses of 100 and 150 μg/kg reversed the increase in BBB leakage induced by MES-induced seizures.
Conclusion: The rhVEGF administration can prevent MES-induced seizures by regulating NO, TAC, and miR-142-5 expression levels in the hippocampus and reducing BBB leakage in mice.
Keywords: Vascular endothelial growth factor, Generalized tonic-clonic seizure, Blood-brain Barrier, microRNAs, mouse, Oxidative stress
Type of Study: Research |
Subject:
General
Received: 2023/06/15 | Accepted: 2023/09/2 | Published: 2024/04/1
Received: 2023/06/15 | Accepted: 2023/09/2 | Published: 2024/04/1
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Articles Copyright © The Author(s).
Owned by Guilan University of Medical Sciences.
Co-published by Negah Institute for Scientific Communication.
Contact Information
Caspian Journal of Neurological Sciences
Guilan University of Medical Sciences
University Tel : +9813 3333 0939
E-mail: cjnsgums@gmail.com, cjns@gums.ac.ir
Owned by Guilan University of Medical Sciences.
Co-published by Negah Institute for Scientific Communication.
Contact Information
Caspian Journal of Neurological Sciences
Guilan University of Medical Sciences
University Tel : +9813 3333 0939
E-mail: cjnsgums@gmail.com, cjns@gums.ac.ir
