Jing Yang1, Xuehua Liu, Yi Zhou, Guozhong Wang, Chunjin Gao, Qingjun Su. 1. *Department of Hyperbaric Oxygen, Beijing Chao-yang Hospital, Capital Medical University, Beijing, China †Department of Orthopaedics, Shen Zhou Hospital Affiliated to Shenyang Medical College, Shenyang, China ‡Department of Hyperbaric Oxygen, Civil Aviation General Hospital, Beijing, China; and §Department of Orthopaedics, Beijing Chao-yang Hospital, Capital Medical University, Beijing, China.
Abstract
STUDY DESIGN: We presented an insight into the effect of hyperbaric oxygen (HBO) on spinal cord injury (SCI), aiming to uncover the dynamics of high-mobility group protein B1 (HMGB1) and nuclear factor κB (NF-κB) after HBO intervention in rats with acute SCI. OBJECTIVE: Prognosis of SCI is directly linked with the control of secondary injury, in which the inflammatory response plays a leading role. HBO therapy can reduce this secondary damage to the spinal cord. We used an animal model to characterize the therapeutic effect of HBO on SCI. SUMMARY OF BACKGROUND DATA: A growing number of studies have confirmed that HBO has gradually become an indispensable element after SCI in reducing neurological disorders, and improving the physical function and quality of life of patients. The role of HBO in the process of HMGB1/NF-κB-related secondary inflammatory responses in SCI has yet to be characterized. METHODS: Rats were randomly categorized into sham, sham + HBO, SCI, and SCI + HBO groups. The expression levels of HMGB1 and NF-κB were measured at days 1, 3, 7, and 14 after SCI. RESULTS: After SCI, significant increases in mRNA and protein expression were observed for both HMGB1 and NF-κB (P< 0.01) compared with sham group. HMGB1 mRNA and protein expression levels were decreased after HBO intervention. The decreases were significant at days 7 and 14 (P< 0.05) post-HBO. In the SCI + HBO group, the significant decreases in NF-κB mRNA and protein expression levels were also observed at days 3, 7, and 14 (P< 0.05). After HBO intervention, a significant increase was seen in the Basso, Beattie, and Bresnahan score at days 7 and 14 (P< 0.05). CONCLUSION: HBO intervention may reduce the secondary damage of SCI caused by inflammatory responses via downregulating the expression of HMGB1/NF-κB, and promoting the repair of neurological function. LEVEL OF EVIDENCE: N/A.
STUDY DESIGN: We presented an insight into the effect of hyperbaric oxygen (HBO) on spinal cord injury (SCI), aiming to uncover the dynamics of high-mobility group protein B1 (HMGB1) and nuclear factor κB (NF-κB) after HBO intervention in rats with acute SCI. OBJECTIVE: Prognosis of SCI is directly linked with the control of secondary injury, in which the inflammatory response plays a leading role. HBO therapy can reduce this secondary damage to the spinal cord. We used an animal model to characterize the therapeutic effect of HBO on SCI. SUMMARY OF BACKGROUND DATA: A growing number of studies have confirmed that HBO has gradually become an indispensable element after SCI in reducing neurological disorders, and improving the physical function and quality of life of patients. The role of HBO in the process of HMGB1/NF-κB-related secondary inflammatory responses in SCI has yet to be characterized. METHODS:Rats were randomly categorized into sham, sham + HBO, SCI, and SCI + HBO groups. The expression levels of HMGB1 and NF-κB were measured at days 1, 3, 7, and 14 after SCI. RESULTS: After SCI, significant increases in mRNA and protein expression were observed for both HMGB1 and NF-κB (P< 0.01) compared with sham group. HMGB1 mRNA and protein expression levels were decreased after HBO intervention. The decreases were significant at days 7 and 14 (P< 0.05) post-HBO. In the SCI + HBO group, the significant decreases in NF-κB mRNA and protein expression levels were also observed at days 3, 7, and 14 (P< 0.05). After HBO intervention, a significant increase was seen in the Basso, Beattie, and Bresnahan score at days 7 and 14 (P< 0.05). CONCLUSION: HBO intervention may reduce the secondary damage of SCI caused by inflammatory responses via downregulating the expression of HMGB1/NF-κB, and promoting the repair of neurological function. LEVEL OF EVIDENCE: N/A.