TY  - JOUR
PY  - 2019//
TI  - Activation of the Nrf2-ARE signal pathway after blast induced traumatic brain injury in mice
JO  - International journal of neuroscience
A1  - Zhou, Yuan
A1  - Tian, Mi
A1  - Wang, Han-Dong
A1  - Gao, Chao-Chao
A1  - Zhu, Lin
A1  - Lin, Yi-Xing
A1  - Fang, Jiang
A1  - Ding, Ke
SP  - 801
EP  - 807
VL  - 129
IS  - 8
N2  - 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>
LA  - en
SN  - 0020-7454
UR  - http://dx.doi.org/10.1080/00207454.2019.1569652
ID  - ref1
ER  -