Vitamin D Receptor Activation Influences NADPH Oxidase (NOX2) Activity and Protects against Neurological Deficits and Apoptosis in a Rat Model of Traumatic Brain Injury
Joint Authors
Jiang, Pei
Cui, Changmeng
Song, Sixin
Cui, Jianzhong
Feng, Yan
Gao, Junling
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2017-12-19
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Traumatic brain injury (TBI) is a worldwide phenomenon which results in significant neurological and cognitive deficits in humans.
Vitamin D (VD) is implicated as a therapeutic strategy for various neurological diseases now.
Recently, inhibition of the NADPH oxidase (NOX2) was reported to protect against oxidative stress (ROS) production.
However, whether alterations in NOX2 expression and NOX activity are associated with calcitriol (active metabolite of VD) treatment following TBI remains unclear.
In the present study, rats were randomly assigned to the sham, TBI, and calcitriol-treated groups.
Calcitriol was administered intraperitoneally (2 μg/kg) at 30 min, 24 h, and 48 h after TBI insult.
We observed that calcitriol treatment alleviated neurobehavioral deficits and brain edema following TBI.
At the molecular levels, administration of calcitriol activated the expression of VDR and downregulated NOX2 as well as suppressed apoptosis cell rate in the hippocampus CA1 region of TBI rats.
In conclusion, our findings indicate that the protective effects of calcitriol may be related to the modulation of NADPH oxidase and thereby ultimately inhibited the progression of apoptosis.
Calcitriol may be promising as a protective intervention following TBI, and more study is warranted for its clinical testing in the future.
American Psychological Association (APA)
Cui, Changmeng& Song, Sixin& Cui, Jianzhong& Feng, Yan& Gao, Junling& Jiang, Pei. 2017. Vitamin D Receptor Activation Influences NADPH Oxidase (NOX2) Activity and Protects against Neurological Deficits and Apoptosis in a Rat Model of Traumatic Brain Injury. Oxidative Medicine and Cellular Longevity،Vol. 2017, no. 2017, pp.1-13.
https://search.emarefa.net/detail/BIM-1196388
Modern Language Association (MLA)
Cui, Changmeng…[et al.]. Vitamin D Receptor Activation Influences NADPH Oxidase (NOX2) Activity and Protects against Neurological Deficits and Apoptosis in a Rat Model of Traumatic Brain Injury. Oxidative Medicine and Cellular Longevity No. 2017 (2017), pp.1-13.
https://search.emarefa.net/detail/BIM-1196388
American Medical Association (AMA)
Cui, Changmeng& Song, Sixin& Cui, Jianzhong& Feng, Yan& Gao, Junling& Jiang, Pei. Vitamin D Receptor Activation Influences NADPH Oxidase (NOX2) Activity and Protects against Neurological Deficits and Apoptosis in a Rat Model of Traumatic Brain Injury. Oxidative Medicine and Cellular Longevity. 2017. Vol. 2017, no. 2017, pp.1-13.
https://search.emarefa.net/detail/BIM-1196388
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1196388