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Copyright (c) 2023 Wei Rong, Huimin Li, Huadong Yang, Bei Yuan, Jianjin Zhu, Jiuzheng Deng, Songhua Xiao, Cheng Zhang
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.Ezetimibe attenuates functional impairment via inhibition of oxidative stress and inflammation in traumatic spinal cord injury
Corresponding Author(s) : Cheng Zhang
Cellular and Molecular Biology,
Vol. 69 No. 6: Issue 6
Abstract
Sustained inflammation after a traumatic spinal cord injury (TSCI) triggers oxidative stress and neuronal apoptosis, hindering functional recovery. Ezetimibe (EZE) has been reported to have anti-inflammatory and antioxidative properties in hepatology-related diseases, but its potential role in SCI remains unclear. In this study, we evaluated the therapeutic effect of EZE on inflammatory microglia and in an SCI model and elucidated the underlying mechanism. First, we stimulated the BV2 microglia cell line with LPS, and we also induced moderate spinal cord injuries in adult male C57BL/6 mice. Both the cells and mice were treated with EZE, and we investigated inflammation, oxidative stress, neurologic damage, and motor function in vitro and in vivo, respectively. Our findings demonstrated that EZE administration attenuates inflammation in microglia by regulating the AMPK/Nrf2 axis. Furthermore, EZE treatment reduced inflammation and oxidative stress levels in the injured spinal cord. Additionally, treatment with EZE decreased glial scarring and improved motor function recovery, indicating the protective role of EZE in SCI. EZE was found to have anti-inflammatory and antioxidative effects on SCI, and it modulated the AMPK/Nrf2 pathway in microglia. Moreover, EZE prevented histological destruction of the spinal cord tissue. In conclusion, EZE shows promise as a drug to protect neurologic integrity following post-SCI.
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