@article{ref1,
title="Activation of the Nrf2-ARE signal pathway after blast induced traumatic brain injury in mice",
journal="International journal of neuroscience",
year="2019",
author="Zhou, Yuan and Tian, Mi and Wang, Han-Dong and Gao, Chao-Chao and Zhu, Lin and Lin, Yi-Xing and Fang, Jiang and Ding, Ke",
volume="129",
number="8",
pages="801-807",
abstract="Background Treatment of blast-induced traumatic brain injury (bTBI) has been hindered. Previous studies have demonstrated that oxidative stress may contribute to the pathophysiological process. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) signaling pathway exhibits a protective effect after traumatic brain injury (TBI). This study explored whether the Nrf2-ARE pathway was activated in a modified bTBI mouse model. <br><br>METHOD Mice were randomly divided into six groups: the 6 h, 1 d, 3 d, 7 d, and 14 d after bTBI groups and a sham group. The protein levels of nuclear Nrf2, heme oxygenase-1 (HO-1), and NAD(P)H: quinone oxidoreductase-1 (NQO1) were detected using western blot, and HO-1 and NQO1 mRNA levels were determined by real-time quantitative polymerase chain reaction. Moreover, HO-1 and Nrf2 were localized using histological staining. <br><br>RESULTS The protein level of the Nrf2-ARE pathway in the frontal lobe increased significantly in the 3 d after bTBI. The HO-1 and NQO1 mRNA levels also reached a peak in the frontal lobe 3 d after bTBI. The histological staining demonstrated higher expression of HO-1 in the frontal lobe and hippocampus 3 d after bTBI, when nuclear import of Nrf2 reached a peak in the frontal lobe. <br><br>CONCLUSIONS bTBI activated the Nrf2-ARE signaling pathway in the brain. The peak activation time in the frontal lobe may be 3 d after injury, and activating the Nrf2 pathway could be a new direction for treatment.<p /> <p>Language: en</p>",
language="en",
issn="0020-7454",
doi="10.1080/00207454.2019.1569652",
url="http://dx.doi.org/10.1080/00207454.2019.1569652"
}