Inhibitory effect of melatonin on cerebral endothelial cells dysfunction induced by methamphetamine via NADPH oxidase-2
作者： Pichaya Jumnongprakhon , Piyarat Govitrapong , Chainarong Tocharus , Jiraporn Tocharus
DOI: 10.1016/J.BRAINRES.2016.08.045
关键词: Neurotoxicity 、 NADPH oxidase 、 Reactive nitrogen species 、 Apocynin 、 Blood–brain barrier 、 Pharmacology 、 Pineal gland 、 Immunology 、 Melatonin 、 Meth- 、 Biology
摘要: Melatonin is a hormone that mostly produced from the pineal gland, and it performs as strong neuroprotectant to both neuron glial cells against methamphetamine (METH)-induced neurotoxicity. Recently, has been found METH also damages blood brain barrier (BBB) structure function. However, protective mechanism of melatonin on BBB impairment caused by not investigated. In this study, primary rat microvascular endothelium (BMVECs) isolated neonatal rats was used investigate effect METH-induced underlying mechanism. The results demonstrated decreased level reactive oxygen species (ROS), nitrogen (RNS), apoptosis induced via NADPH oxidase (NOX)-2 since apocynin, NOX-2 inhibitor abolished those changes. addition, improve cell integrity increasing transendothelial electric resistance (TEER) values, up-regulate tight junction proteins ZO-1, occludin, claudin-5, thereby decreasing paracellular permeability mediated NOX-2. Our data suggest induces mediating activity, then oxidative nitrative stress, well apoptosis, which causes integrity, reduces these negative effects MT1/2 receptors.
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