Inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via NADPH oxidase-2

© 2016 Elsevier B.V. Melatonin is a hormone that mostly produced from the pineal gland, and it performs as a strong neuroprotectant to both neuron and glial cells against methamphetamine (METH)-induced neurotoxicity. Recently, it has been found that METH also damages the blood brain barrier (BBB) st...

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Main Authors: Pichaya Jumnongprakhon, Piyarat Govitrapong, Chainarong Tocharus, Jiraporn Tocharus
Format: Journal
Published: 2018
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http://cmuir.cmu.ac.th/jspui/handle/6653943832/55130
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Institution: Chiang Mai University
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spelling th-cmuir.6653943832-551302018-09-05T03:11:35Z Inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via NADPH oxidase-2 Pichaya Jumnongprakhon Piyarat Govitrapong Chainarong Tocharus Jiraporn Tocharus Biochemistry, Genetics and Molecular Biology Medicine Neuroscience © 2016 Elsevier B.V. Melatonin is a hormone that mostly produced from the pineal gland, and it performs as a strong neuroprotectant to both neuron and glial cells against methamphetamine (METH)-induced neurotoxicity. Recently, it has been found that METH also damages the blood brain barrier (BBB) structure and function. However, the protective mechanism of melatonin on the BBB impairment caused by METH has not been investigated. In this study, the primary rat brain microvascular endothelium cells (BMVECs) isolated from neonatal rats was used to investigate the protective effect of melatonin on METH-induced BBB impairment and the underlying mechanism. The results demonstrated that melatonin decreased the level of reactive oxygen species (ROS), reactive nitrogen species (RNS), and apoptosis induced by METH via NADPH oxidase (NOX)-2 since apocynin, a NOX-2 inhibitor abolished those changes. In addition, melatonin was found to improve cell integrity by increasing the transendothelial electric resistance (TEER) values, and up-regulate the tight junction proteins ZO-1, occludin, and claudin-5, thereby decreasing the paracellular permeability caused by METH mediated by NOX-2. Our data suggest that METH induces BBB impairment by mediating NOX-2 activity, and then induces oxidative and nitrative stress, as well as apoptosis, which causes the impairment of cell integrity, and that melatonin reduces these negative effects of METH by mediating via MT1/2 receptors. 2018-09-05T02:52:07Z 2018-09-05T02:52:07Z 2016-11-01 Journal 18726240 00068993 2-s2.0-84986236309 10.1016/j.brainres.2016.08.045 https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84986236309&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/55130
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
collection CMU Intellectual Repository
topic Biochemistry, Genetics and Molecular Biology
Medicine
Neuroscience
spellingShingle Biochemistry, Genetics and Molecular Biology
Medicine
Neuroscience
Pichaya Jumnongprakhon
Piyarat Govitrapong
Chainarong Tocharus
Jiraporn Tocharus
Inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via NADPH oxidase-2
description © 2016 Elsevier B.V. Melatonin is a hormone that mostly produced from the pineal gland, and it performs as a strong neuroprotectant to both neuron and glial cells against methamphetamine (METH)-induced neurotoxicity. Recently, it has been found that METH also damages the blood brain barrier (BBB) structure and function. However, the protective mechanism of melatonin on the BBB impairment caused by METH has not been investigated. In this study, the primary rat brain microvascular endothelium cells (BMVECs) isolated from neonatal rats was used to investigate the protective effect of melatonin on METH-induced BBB impairment and the underlying mechanism. The results demonstrated that melatonin decreased the level of reactive oxygen species (ROS), reactive nitrogen species (RNS), and apoptosis induced by METH via NADPH oxidase (NOX)-2 since apocynin, a NOX-2 inhibitor abolished those changes. In addition, melatonin was found to improve cell integrity by increasing the transendothelial electric resistance (TEER) values, and up-regulate the tight junction proteins ZO-1, occludin, and claudin-5, thereby decreasing the paracellular permeability caused by METH mediated by NOX-2. Our data suggest that METH induces BBB impairment by mediating NOX-2 activity, and then induces oxidative and nitrative stress, as well as apoptosis, which causes the impairment of cell integrity, and that melatonin reduces these negative effects of METH by mediating via MT1/2 receptors.
format Journal
author Pichaya Jumnongprakhon
Piyarat Govitrapong
Chainarong Tocharus
Jiraporn Tocharus
author_facet Pichaya Jumnongprakhon
Piyarat Govitrapong
Chainarong Tocharus
Jiraporn Tocharus
author_sort Pichaya Jumnongprakhon
title Inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via NADPH oxidase-2
title_short Inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via NADPH oxidase-2
title_full Inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via NADPH oxidase-2
title_fullStr Inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via NADPH oxidase-2
title_full_unstemmed Inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via NADPH oxidase-2
title_sort inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via nadph oxidase-2
publishDate 2018
url https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84986236309&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/55130
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