IMR Press / JIN / Volume 18 / Issue 2 / DOI: 10.31083/j.jin.2019.02.120
Open Access Original Research
β-carotene provides neuroprotection after experimental traumatic brain injury via the Nrf2-ARE pathway
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1 Shanghai University of Medicine and Health Sciences, Shanghai 201318, P. R. China
2 Tai'an City Central Hospital, Taian 271000, P. R. China
3 Shanghai University of Traditional Chinese Medicine, Shanghai 201318, P. R. China
4 School of Pharmaceutical Science, Taishan Medical University, Taian 271000, P. R. China
5 Affiliated Health School of Shanghai University of Medicine and Health Sciences, Shanghai, 201318, P. R. China
*Correspondence: (Xiamin Hu); (Xiaoming Xin)
#These authors contributed equally.
J. Integr. Neurosci. 2019, 18(2), 153–161;
Submitted: 17 January 2018 | Accepted: 8 May 2019 | Published: 30 June 2019
Copyright: © 2019 Chen et al. Published by IMR press.
This is an open access article under the CC BY-NC 4.0 license (

We investigate whether β-carotene, a known natural antioxidant, can reduce oxidative stress induced by traumatic brain injury. In addition, we investigated the underlying mechanism of traumatic brain injury focusing on the NF-E2-related factor (Nrf2) pathway. A controlled cortical impact model was used to mimic traumatic brain injury. Using this model, we evaluated brain edema, lesion volume, neurologic deficits, reactive oxygen species, and the expression of Nrf2-related protein markers. The results of our study demonstrated that cognitive performance and neural functions were improved with β-carotene administration. In addition, β-carotene reduced brain edema and reactive oxygen species levels after traumatic brain injury. Nrf2 nuclear accumulation was increased and was accompanied by decreased Keap1 expression. The expression of quinone oxidoreductase 1, a target gene of the Nrf2 signaling pathway was increased. However, lesion volume was not significantly reduced after β-carotene treatment. Taken together, our data demonstrated that β-carotene administration was neuroprotective and alleviated oxidative stress by modulating the Nrf2/Keap1mediated antioxidant pathway in the traumatic brain injury model.

Traumatic brain injury
oxidative stress
Nrf2-ARC signaling pathway
mouse model
Figure 1.
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