Vitamin D Receptor Activation Influences NADPH Oxidase (NOX(2)) Activity and Protects against Neurological Deficits and Apoptosis in a Rat Model of Traumatic Brain Injury.
Vitamin D Receptor Activation Influences NADPH Oxidase (NOX(2)) Activity and Protects against Neurological Deficits and Apoptosis in a Rat Model of Traumatic Brain Injury.
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DOI：
10.1155/2017/9245702
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发表时间：
2017
影响因子：
--
通讯作者：
Jiang P
中科院分区：
文献类型：
--
作者：
Cui C;Song S;Cui J;Feng Y;Gao J;Jiang P
创伤性脑损伤（TBI）是一种世界性的现象，其导致人类显著的神经和认知缺陷。维生素D（VD）是目前治疗多种神经系统疾病的有效药物。最近，据报道抑制NADPH氧化酶（NOX 2）可以防止氧化应激（ROS）的产生。然而，NOX 2表达和NOX活性的改变是否与TBI后骨化三醇（VD的活性代谢物）治疗相关仍不清楚。在本研究中，将大鼠随机分配至假手术组、TBI组和骨化三醇治疗组。在TBI损伤后30分钟、24小时和48小时腹膜内施用骨化三醇（2 μg/kg）。我们观察到骨化三醇治疗减轻了TBI后的神经行为缺陷和脑水肿。在分子水平上，骨化三醇可激活TBI大鼠海马CA 1区VDR的表达，下调NOX 2的表达，抑制凋亡细胞的发生。总之，我们的研究结果表明，骨化三醇的保护作用可能与NADPH氧化酶的调制，从而最终抑制细胞凋亡的进展。骨化三醇可能是一种有前途的保护性干预TBI后，和更多的研究是必要的，在未来的临床试验。
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.
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影响因子：
9.3
作者：
Dohi K;Ohtaki H;Nakamachi T;Yofu S;Satoh K;Miyamoto K;Song D;Tsunawaki S;Shioda S;Aruga T
通讯作者：
Aruga T
影响因子：
5.9
作者：
Jiang P;Zhang LH;Cai HL;Li HD;Liu YP;Tang MM;Dang RL;Zhu WY;Xue Y;He X
通讯作者：
He X
影响因子：
3.4
作者：
Fu, Jun;Xue, Rui;Ran, Ran
通讯作者：
Ran, Ran
影响因子：
3.3
作者：
Cui, Changmeng;Cui, Ying;Cui, Jianzhong
通讯作者：
Cui, Jianzhong
影响因子：
4.2
作者：
Chabas, Jean-Francois;Alluin, Olivier;Feron, Francois
通讯作者：
Feron, Francois