Hyperbaric oxygen improves functional recovery of rats after spinal cord injury via activating strom

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Background:Spinal cord injury (SCI) is a worldwide medical conc.This study aimed to elucidate the mechanism underlying the protective effect of hyperbaric oxygen (HBO) against SCI-induced neurologic defects in rats via exploring the stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4) axis and expression of brain-derived neurotrophic factor (BDNF).Methods:An acute SCI rat model was established in Sprague-Dawley rats using the Allen method.Sixty rats were divided into four groups (n=15 in each group):sham-operated,SCI,SCI treated with HBO (SCI+HBO),and SCI treated with both HBO and AMD3100 (an antagonist of CXCR4;SCI+HBO+AMD) groups.The rats were treated with HBO twice a day for 3 days and thereafter once a day after the surgery for up to 28 days.Following the surgery,neurologic assessments were performed with the Basso-Bettie-Bresnahan (BBB) scoring system on postoperative day (POD) 7,14,21,and 28.Spinal cord tissues were harvested to assess the expression of SDF-1,CXCR4,and BDNF at mRNA and protein levels,using quantitative real-time polymerase chain reaction,West blot analysis,and histopathologic analysis.Results:HBO treatment recovered SCI-induced descent of BBB scores on POD 14,(1.25 ± 0.75 vs.1.03 ± 0.66,P < 0.05),21 (5.27 ± 0.89 vs.2.56 ± 1.24,P < 0.05),and 28 (11.35 ± 0.56 vs.4.23 ± 1.20,P < 0.05) compared with the SCI group.Significant differences were found in the mRNA levels of SDF-1 (mRNA:day 21,SCI + HBO vs.SCI + HBO + AMD,2.89 ± 1.60 vs.1.56 ± 0.98,P < 0.05),CXCR4 (mRNA:day 7,SCI+ HBO vs.SCI,2.99± 1.60 vs.1.31 ±0.98,P< 0.05;day 14,SCI+ HBO vs.SCI+HBO +AMD,4.18± 1.60 vs.0.80±0.34,P< 0.05;day 21,SCI+HBO vs.SCI,2.10±1.01 vs.1.15 ±0.03,P<0.05),and BDNF (mRNA:day 7,SCI+ HBO vs.SCI,3.04 ± 0.41 vs.2.75 ± 0.31,P < 0.05;day 14,SCI + HBO vs.SCI,3.88 ± 1.59 vs.1.11 ± 0.40,P < 0.05),indicating the involvement of SDF-1/CXCR4 axis in the protective effect of HBO.Conclusions:HBO might promote the recovery of neurologic function after SCI in rats via activating the SDF-1/CXCR4 axis and promoting BDNF expression.
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