Protective effect of edaravone on blood-brain barrier by affecting NRF-2/HO-1 signaling pathway
- Jing Liu
- Yan Jiang
- Guangping Zhang
- Zaihong Lin
- Shu Du
Affiliations: Fourth Department of Neurology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang 161000, P.R. China
- Published online on: August 6, 2019 https://doi.org/10.3892/etm.2019.7859
Copyright: © Liu
et al. This is an open access article distributed under the
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Protective effect of edaravone on blood-brain barrier (BBB) in experimental cerebral infarction rats was investigated. SD rats were prepared as the permanent middle cerebral artery occlusion model and randomly divided into 4 groups: cerebral infarction model group, edaravone low, medium and high dose groups. Healthy rats only for operation and no filament were selected as the sham operation control group. Rats in the cerebral infarction model group and the control group were given normal saline, and those in the edaravone low, medium and high dose groups were given edaravone 10, 15 and 20 mg/kg, respectively. The survival status, the body weight and neurological function score before and after treatment, the brain water content and the permeability of the blood-brain barrier after treatment were measured. The expression levels of NFE2-related factor 2 (NRF2) and hemeoxygenase 1 (HO-1) in rat brain tissue were detected by western blotting. Levels of peripheral blood malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) were detected by ELISA. The state of the rats in three edaravone groups was improved compared with that of the cerebral infarction group. Compared with the cerebral infarction model group, the body weight was significantly increased after treatment and the neurological function score, brain tissue water content and BBB permeability were significantly decreased in three edaravone groups (P<0.05).Compared with the model group of cerebral infarction, the expression of NRF-2 and HO-1 in the brain of the three edaravone groups was significantly higher (P<0.05). Compared with the model group of cerebral infarction, the expression of MDA and GSH in the three edaravone groups was significantly decreased, GSH and SOD was increased (P<0.05), in a dose-dependent manner. Edaravone might play a protective role in the BBB by activating the NRF-2/HO-1 signaling pathway.