title: Effects of hyperbaric oxygen therapy on RAGE and MCP-1 expression in rats with spinal cord injury.
abstract: The inflammatory response is an important source of secondary damage to neuronal tissue in the spinal cord following spinal cord injury (SCI). Hyperbaric oxygen (HBO) therapy reduces inflammation and promotes the restoration of locomotor function following SCI, however, the mechanisms underlying this effect remain to be determined. The aim of the current study was to investigate the mechanisms by which HBO therapy promotes recovery in a rat model of SCI by measuring expression levels of receptor for advanced glycation end products (RAGE) and monocyte chemoattractant protein‑1 (MCP‑1) in spinal cord tissue. Experimental animals (n=90) were divided into three groups: Sham‑operated (SH), SCI (T‑10 laminectomy) and SCI + HBO. Each group was further divided into five subgroups (n=6) that were examined at 12 h, and at 1, 3, 7 and 14 days post‑injury. Recovery of locomotor function was evaluated using the Basso, Beattie and Bresnahan (BBB) scoring system. Neutrophil infiltration was analyzed using myeloperoxidase (MPO) activity assays. The expression of RAGE and MCP‑1 was measured by immunohistochemistry, reverse transcription‑quantitative polymerase chain reaction and western blotting. RAGE and MCP‑1 expression and MPO activity were higher in the SCI groups than in the SH groups at each time point. HBO therapy reduced RAGE and MCP‑1 expression and MPO activity compared with untreated, injured animals at early post‑injury stages. In addition, HBO therapy improved BBB scores at post‑operative day 7 and 14. HBO therapy was, therefore, demonstrated to relieve secondary inflammatory responses, potentially by inhibiting the expression of RAGE and MCP‑1, resulting in significant recovery of locomotor function. The results of the present study may, therefore, be useful in improving the clinical application of HBO therapy for patients with SCI.
authors.affiliation: Department of Emergency, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Emergency, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Chunsheng
authors.initials: C
authors.lastname: Li
authors.affiliation: Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Chunjin
authors.initials: C
authors.lastname: Gao
authors.affiliation: Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Zhuo
authors.initials: Z
authors.lastname: Li
authors.affiliation: Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Jing
authors.initials: J
authors.lastname: Yang
authors.affiliation: Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Xuehua
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Hyperbaric Oxygen, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, P.R. China.
authors.forename: Fang
authors.initials: F
authors.lastname: Liang
mesh_terms: D000818:Animals; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D015870:Gene Expression; D006931:Hyperbaric Oxygenation; D007150:Immunohistochemistry; D009043:Motor Activity; D020556:Neutrophil Infiltration; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D000067759:Receptor for Advanced Glycation End Products / Q000235:genetics / Q000378:metabolism*; D020127:Recovery of Function; D013119:Spinal Cord Injuries / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000628:therapy
chemical_list: D018932:Chemokine CCL2; D000067759:Receptor for Advanced Glycation End Products; D009195:Peroxidase