Influence of hypoxic preconditioning in anti-oxidative ability and neurological functions in traumatic brain injury rats

Abstract

Objective To research the influence of hypoxic preconditioning in anti-oxidative ability of brain tissues and neurological functions in rats after traumatic brain injury.Methods Forty eight adult male Sprague Dawley rats were randomly divided into sham-operated group,hypoxic preconditioning group (HPC),traumatic brain injury group (TBI) and hypoxic preconditioning+traumatic brain injury group (HPCT,n=12).The HPC rat models were made by hypobaric chamber for 3 d (50 kPa,3 h/d) and TBI were induced by Feeney's improved equipment.All rats were killed 24 h after injury,and the neurological functions of each group were evaluated by modified neurologieal severity scale (mNSS);the neuronal survival around contusion area was detected by NeuN immunohistochemical staining,and the protein and mRNA expressions of nuclear transcription factor-related factor 2 (Nrf2) and thioredoxin reductases 2 (TrxR2) in the brain tissues were detected by Western blotting and real-time quantitative PCR.Results The mNSS scores in the TBI and HPCT groups were significantly higher as compared with those in the sham-operated and HPC groups (P＜0.05),but those in the HPCT group was significantly lower than those in the TBI group (P＜0.05).The neuronal survival in the TBI and HPCT groups was decreased as compared with that in the sham-operated and HPC groups (NeuN expressions:0.274±0.033,0.281±0.042 vs 0.124±0.014,0.150±0.019),with significant difference (P＜0.05),while that in the HPCT group was statistically increased as compared with that in the TBI group (P＜0.05).The expressions of Nrf2 and TrxR2 in the brain tissues of TBI and HPCT groups were significantly increased as compared with those in the sham-operated and HPC groups (P＜0.05),and those in the HPCT group was significantly up-regulated as compared with those in the TBI group (P＜0.05).Conclusion HPC can increase the anti-oxidative ability and relieve the neurological functions missing after TBI. Key words: Traumatic brain injury; Nuclear factor erythroid 2-related factor 2; Thioredoxin reductases 2; Hypoxic preconditioning