The neuroprotection of hypoxic preconditioning on rat brain against traumatic brain injury by up-regulated transcription factor Nrf2 and HO-1 expression. (12th January 2016)

• Record Type: Journal Article
• Authors: Shu, Longfei; Wang, Chunlin; Wang, Jinbiao; Zhang, Yongming; Zhang, Xing; Yang, Yanyan; Zhuo, Jianwei; Liu, Jiachuan
• Is Part Of: Neuroscience letters. Volume 611(2016)
• Page Start: 74
• Page End: 80
• Publication Date: 2016-01-12
• Subjects: Traumatic brain injury -- Hypoxic preconditioning -- Nuclear factor erythroid 2-related factor 2p -- Heme oxygenase-1; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.11.012
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Hypoxic preconditioning was induced on rat by using a hypobaric chamber. Hypoxic training (360 Torr, 3 h/d, 3 d) conferred neuroprotective effects on the rat's brain against TBI. Hypoxic training (360 Torr, 3 h/d, 3 d) significantly increased the Nrf2 signaling activation after TBI. Abstract: Hypoxic preconditioning (HPC) increases the inherent tolerance of brain tissue suffering from severe hypoxia or ischemia insult by stimulating the protective ability of the brain. However, little is known concerning the effect of HPC on traumatic brain injury (TBI). We designed this study to investigate the effect of HPC on TBI and explore its underlying mechanisms. We found that HPC significantly alleviates neurological dysfunction, lessens brain edema, reduces cell apoptosis, increases neuronal survival, up-regulates the expressions of Nrf2 and HO-1, and decreases the inducer of protein carbonyls, 4-hydroxy-2-nonenal, and 8-hydroxy-2-deoxyguanosine in the brain tissue of rats 24 h after brain injury. However, no influence was observed in normal rats after only 3 d of hypoxic training. Results further indicated that HPC protects the brain against traumatic damage. This protective effect may be achieved by up-regulating Nrf2 and HO-1 expression and alleviating oxidative stress damage.