• Feng Li, Jing Liang, and Dongfang Tang.
• Anesthesiology Department, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 277 West Yanta Road, Shaanxi Province, 710061, China. Electronic address: doctorlifeng@xjtu.edu.cn.
• Biomed. Pharmacother. 2018 Dec 1; 108: 1216-1224.

AbstractAccumulating evidence suggests that brahma-related gene 1 (Brg1) is a critical regulator of cell apoptosis and oxidative stress in response to various insults; however, whether Brg1 regulates neuronal apoptosis and oxidative stress during cerebral ischemia/reperfusion injury remains unclear. This study aimed to investigate the expression, biological function, and regulatory mechanism of Brg1 in regulating neuronal apoptosis and oxidative stress induced by oxygen-glucose deprivation/reoxygenation (OGD/R), an in vitro cellular model of cerebral ischemia and reperfusion injury. The results showed that Brg1 expression was altered in response to OGD/R treatment. Overexpression of Brg-1 increased cell viability, attenuated apoptosis, and reduced reactive oxygen species (ROS) production in neurons, thus showing a protective effect against OGD/R-induced injury. In contrast, knockdown of Brg1 significantly inhibited cell viability, increased apoptosis, and promoted ROS production in neurons following OGD/R treatment. Moreover, these results showed that Brg1 promoted the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and increased the expression of heme oxygenase-1 (HO-1). However, knockdown of Nrf2 or HO-1 significantly abrogated Brg1-mediated neuroprotective effects. Taken together, these results demonstrate that Brg1 ameliorates OGD/R-induced neuronal injury in vitro by promoting the activation of Nrf2/HO-1 signaling. The study highlights a potential role of Brg1 in regulating cerebral ischemia/reperfusion injury in vivo.Copyright © 2018 Elsevier Masson SAS. All rights reserved.

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