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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 9245702, 13 pages
https://doi.org/10.1155/2017/9245702
Research Article

Vitamin D Receptor Activation Influences NADPH Oxidase (NOX2) Activity and Protects against Neurological Deficits and Apoptosis in a Rat Model of Traumatic Brain Injury

1Department of Neurosurgery, Affiliated Hospital of Jining Medical University, Jining, Shandong 272000, China
2School of Basic Medical Science, North China University of Science and Technology, Tangshan, Hebei 063000, China
3Department of Neurosurgery, Tangshan Gongren Hospital, Tangshan, Hebei 063000, China
4Department of Neurosurgery, Affiliated Hospital of Taishan Medical University, Taian, Shandong 271000, China
5Department of Neurosurgery, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China
6Institute of Clinical Pharmacy and Pharmacology, Jining First People’s Hospital, Jining Medical University, Jining, Shandong 272000, China

Correspondence should be addressed to Junling Gao; moc.361@1002rdoaglj and Pei Jiang; moc.anis@usciepgnaij

Received 5 April 2017; Revised 18 July 2017; Accepted 30 July 2017; Published 19 December 2017

Academic Editor: Arsenio Fernández-López

Copyright © 2017 Changmeng Cui et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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.