β-Caryophyllene protectsin vitroneurovascular unit against oxygen-glucose deprivation and re-oxygenation-induced injury
| Autor: | Jinwei Pang, Minghang Li, Zhi Dong, Jianjun Zhong, Xiaocui Tian, Mei Yang, Jianhua Peng, Jie Lou, Ruidi An, Lu Xu, Qian Zhang |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Ischemia Context (language use) Biology Pharmacology Blood–brain barrier Occludin medicine.disease_cause Biochemistry Neuroprotection Proinflammatory cytokine Rats Sprague-Dawley 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine medicine Animals Cells Cultured Neurons Polycyclic Sesquiterpenes Anti-Inflammatory Agents Non-Steroidal medicine.disease Cell Hypoxia Rats Oxygen Glucose Neuroprotective Agents 030104 developmental biology medicine.anatomical_structure Animals Newborn nervous system Microvessels Endothelium Vascular Sesquiterpenes Neuroscience 030217 neurology & neurosurgery Homeostasis Oxidative stress |
| Zdroj: | Journal of Neurochemistry. 139:757-768 |
| ISSN: | 0022-3042 |
| Popis: | β-caryophyllene (BCP) mediates neuroprotection in cerebral ischemic animals. The neurovascular unit (NVU) acts as an intricate network to maintain the neuronal homeostatic microenvironment. However, the effects exerted by BCP on NVU remain unclear. Therefore, we established an in vitro NVU model to investigate the effects of BCP on oxygen-glucose deprivation and re-oxygenation (OGD/R)-induced injury. This model involved the co-culture of brain microvascular endothelial cells (BMECs), neurons and astrocytes. BCP (10 μmol/L) was applied for 24 hours prior to OGD/R and maintained throughout OGD/R. Blood-brain barrier (BBB) integrity and neuronal apoptosis were analysed. BCP pretreatment prior to the initiation of OGD/R significantly (i) decreased BBB permeability and neuronal apoptosis, (ii) mitigated oxidative stress damage and the release of inflammatory cytokines, (iii) down-regulated Bax expression, MMP-9 activity and expression, and (iv) up-regulated claudin-5, occludin, ZO-1, GAP-43 and Bcl-2 expression. Thus, BCP pretreatment exerted multiple protective effects on NVU in the context of OGD/R-induced injury. These protective effects potentially occur via reductions in oxidative stress damage and inflammatory cytokines that induce BBB breakdown, subsequently resulting in reduced neuronal apoptosis. NVU serve as putative therapeutic targets for cerebral ischemia, and the results of this study provide new insights for the application of BCP as a neuroprotective agent. This article is protected by copyright. All rights reserved. |
| Databáze: | OpenAIRE |
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