Hyperbaric oxygen improves functional recovery of rats after spinal cord injury via activating stromal cell-derived factor-1/CXC chemokine receptor 4 axis and promoting brain-derived neurothrophic factor expression.
10.1097/CM9.0000000000000115
- Author:
Xiang-Long MENG
1
;
Yong HAI
1
;
Xi-Nuo ZHANG
1
;
Yun-Sheng WANG
1
;
Xue-Hua LIU
2
;
Lin-Lin MA
2
;
Rong YUE
3
;
Gang XU
1
;
Zhuo LI
2
Author Information
1. Orthopedic Department, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
2. Hyperbaric Oxygen Department, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
3. Hyperbaric Oxygen Department, Xinjiang Uygur Autonomous Region People's Hospital, Urumqi, Xinjiang 830001, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Blotting, Western;
Brain-Derived Neurotrophic Factor;
metabolism;
Disease Models, Animal;
Hyperbaric Oxygenation;
methods;
Male;
Rats;
Rats, Sprague-Dawley;
Receptors, CXCR4;
metabolism;
Receptors, Interleukin-8A;
metabolism;
Spinal Cord Injuries;
metabolism;
therapy
- From:
Chinese Medical Journal
2019;132(6):699-706
- CountryChina
- Language:English
-
Abstract:
BACKGROUND:Spinal cord injury (SCI) is a worldwide medical concern. 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, Western 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.
