NDLI: Dl-3-n-Butylphthalide (NBP) Provides Neuroprotection in the Mice Models After Traumatic Brain Injury via Nrf2-ARE Signaling Pathway

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Dl-3-n-Butylphthalide (NBP) Provides Neuroprotection in the Mice Models After Traumatic Brain Injury via Nrf2-ARE Signaling Pathway

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Dl-3-n-Butylphthalide (NBP) Provides Neuroprotection in the Mice Models After Traumatic Brain Injury via Nrf2-ARE Signaling Pathway

Content Provider	Springer Nature Link
Author	Liu, Zhengwei Wang, Handong Shi, Xiaofeng Li, Liwen Zhou, Mengliang Ding, Hui Yang, Youqing Li, Xiang Ding, Ke
Copyright Year	2017
Abstract	The present study was aimed to evaluate the neuroprotective effects of NBP in the mice models of TBI, as well as the possible role of Nrf2-ARE pathways in the assumptive neuroprotection. In mice,a modified Marmarou’s weight-drop model was employed to induce TBI. ICR mice were randomly assigned to four experimental groups: sham, TBI, TBI+vehicle(V) and TBI+NBP. NBP (100 mg/kg) was administered via an intraperitoneal (i.p.) injection at 1 h following TBI. The administration of NBP significantly ameliorated the effects of the brain injury, including neurological deficits, brain water content, and cortical neuronal apoptosis. Furthermore, the level of malondialdehyde and the activity of superoxide dismutase (SOD) paired with glutathione peroxidase (GPx) were restored in the NBP treatment group. NBP promoted the translocation of Nrf2 protein from the cytoplasm to the nucleus markedly, increased the expressions of Nrf2-ARE pathway-related downstream factors, including hemeoxygenase-1(HO-1) and NAD(P)H: quinone oxidoreductase 1 (NQO1), and prevented the decline of antioxidant enzyme activities, including SOD and GPx. NBP enhanced the translocation of Nrf2 to the nucleus from the cytoplasm,verified by a western blot, immunofluorescence. Additionally, it upregulated the expression of the Nrf2 downstream factors such as HO-1 and NQO1 were also confirmed via a western blot and real-time quantitative polymerase chain reaction. In conclusion, NBP administration may increase the activities of antioxidant enzymes and attenuate brain injury in a TBI model, potentially via the mediation of the Nrf2-ARE pathway.
Starting Page	1375
Ending Page	1386
Page Count	12
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	42
Issue Number	5
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2017-02-18
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	dl-3-n-Butylphthalide Neuroprotection Traumatic brain injury Nrf2-ARE signaling pathway Mice model Neurosciences Neurochemistry Biochemistry Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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Dl-3-n-Butylphthalide (NBP) Provides Neuroprotection in the Mice Models After Traumatic Brain Injury via Nrf2-ARE Signaling Pathway