Literature DB >> 24966901

Protective effects of hyperbaric oxygen treatment against spinal cord injury in rats via toll-like receptor 2/nuclear factor-κB signaling.

Jiewen Tan1, Fang Zhang2, Fang Liang3, Yong Wang4, Zhuo Li3, Jing Yang3, Xuehua Liu3.   

Abstract

Spinal cord injury (SCI) is a serious medical problem with high mortality and disability rates. Hyperbaric oxygen (HBO) treatment is beneficial for neurological recovery after SCI, but the underlying mechanisms await characterization. This study examined whether HBO treatment following SCI in rats exerts a neuroprotective effect through activation of the toll-like receptor (TLR) 2/nuclear factor (NF)-κB signaling pathway. The SC of rats was injured via T10 laminectomy. Experimental animals (n=144) were divided into four groups: sham-operated (SH), SH+HBO, SCI, and SCI+HBO. Each group was subdivided into six subgroups (n=6 per group) that were examined at 12 h, and 1, 2, 3, 7, and 14 days post-injury. Functional recovery in the hind limb was evaluated using the Basso, Beattie, and Bresnahan (BBB) scoring system. The expression of TLR2 and NF-кB was assessed by real-time polymerase chain reaction and Western blotting, while interleukin-1 (IL)-1β and tumor necrosis factor (TNF)-α levels were measured by enzyme-linked immunosorbent assay. TLR2 and NF-кB levels and histological scores were higher in the SCI than in the SH and SH+HBO groups at various time points. HBO treatment decreased TLR2 and NF-кB expression and histological scores as well as IL-1β and TNF-α levels compared to the SCI group at early post-injury stages. In addition, BBB scores were improved in the SCI+HBO relative to the SCI group at 7 and 14 days. HBO treatment may mitigate secondary injury to the SC by inhibiting inflammatory responses induced by TLR2/NF-кB signaling, thereby promoting functional recovery and improving neurological outcome.

Entities:  

Keywords:  Hyperbaric oxygen; nuclear factor κB; spinal cord injury; toll-like receptor 2

Mesh:

Substances:

Year:  2014        PMID: 24966901      PMCID: PMC4069961     

Source DB:  PubMed          Journal:  Int J Clin Exp Pathol        ISSN: 1936-2625


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