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作者

Chen, PQ Li, L Gao, YF Xie, ZQ Zhang, Y Pan, ZJ Tu, YX Wang, H Han, QQ Hu, XM Xin, XM ...更多内容...更少内容

作者单位

Taishan Med Univ, Sch Pharmaceut Sci, Tai An 271000, Shandong, Peoples R China        Shandong First Medical University & Shandong Academy of Medical Sciences        Shanghai Univ Tradit Chinese Med, Shanghai 201318, Peoples R China        Shanghai University of Traditional Chinese Medicine Shanghai Univ Med & Hlth Sci, Affiliated Hlth Sch, Shanghai 201318, Peoples R China Shanghai Univ Med & Hlth Sci, Shanghai 201318, Peoples R China        Taian City Cent Hosp, Tai An 271000, Shandong, Peoples R China

刊名

JOURNAL OF INTEGRATIVE NEUROSCIENCE

年份

2019

卷号

Vol.18 No.2

页码

153-161

ISSN

0219-6352

关键词

OXIDATIVE STRESS APOPTOSIS MELATONIN MODEL THERAPY DISEASE MICE

摘要

We investigate whether beta-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 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 resul...更多

We investigate whether beta-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 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 beta-carotene administration. In addition, beta-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 beta-carotene treatment. Taken together, our data demonstrated that beta-carotene administration was neuroprotective and alleviated oxidative stress by modulating the Nrf2/Keap1-mediated antioxidant pathway in the traumatic brain injury model.收起

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