Open Accessβ-carotene provides neuro protection after experimental traumatic brain injury via the Nrf2–ARE pathway
Author(s) -
Peiqing Chen,
Lin Li,
Yue Gao,
Zailai Xie,
Yin Zhang,
Zhoujia Pan,
Yingxin Tu,
Hu Wang,
Qiu-Qin Han,
Xingjian Hu,
Xiaoming Xin
Publication year - 2019
Publication title -
journal of integrative neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.336
H-Index - 33
eISSN - 1757-448X
pISSN - 0219-6352
DOI - 10.31083/j.jin.2019.02.120
Subject(s) - traumatic brain injury , neuroprotection , oxidative stress , keap1 , reactive oxygen species , lesion , antioxidant , brain edema , pharmacology , medicine , neuroscience , chemistry , anesthesia , biology , pathology , biochemistry , gene , transcription factor , psychiatry
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/Keap1- mediated antioxidant pathway in the traumatic brain injury model.