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Copyright (c) 2022 Xue Yang, Bo Wang, Youming Wang
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Keap1-Nrf2/ARE Pathway-based Investigation into the Mechanism of Edaravone Dexborneol in Cerebral Infarction Model Neuroprotection
Corresponding Author(s) : Youming Wang
Cellular and Molecular Biology,
Vol. 68 No. 9: Issue 9
Abstract
The neuroprotection of acute cerebral infarction (ACI) model by edaravone dexborneol (ED)-mediated Keap1-Nrf2/ARE signal pathway was investigated. Sham operation was set as a control to prepare the ACI model with cerebral artery occlusion. The abdominal cavity was injected with edaravone (ACI+Eda group) and ED (ACI+ED group). Then, neurological deficit scores, cerebral infarct volume, oxidative stress ability, inflammatory reaction level, and the status of the Keap1-Nrf2/ARE signal pathway of rats in all groups were explored. It was demonstrated that the neurological deficit score and cerebral infarct volume of rats in the ACI group apparently increased versus those in the Sham group (P<0.05), suggesting that the ACI model was successfully prepared. Versus those in the ACI group, the neurological deficit score and cerebral infarct volume of rats in the ACI+Eda and ACI+ED groups decreased. In contrast, the activity of cerebral oxidative stress superoxide dismutase (SOD) and glutathione-peroxidase (GSH-Px) increased. Malondialdehyde (MDA) and the expressions of cerebral inflammation indicators (interleukin (IL)-1β, IL-6, and tumor necrosis factor-α messenger ribonucleic acid (TNF-α mRNA)) and cerebral Keap1 reduced. The expressions of Nrf2 and ARE increased (P<0.05). Versus those in the ACI+Eda group, all indicators of rats in the ACI+ED group were improved more apparently and were more similar to those in the Sham group (P<0.05). The above findings suggested that both edaravone and ED could mediate Keap1-Nrf2/ARE signal pathway to play a neuroprotective role in ACI. Versus edaravone, ED improved ACI oxidative stress and inflammatory reaction level and played a neuroprotective role more apparently.
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