Expression of inflammatory factors in model rats with acute incomplete spinal cord injury / 中国组织工程研究

ABSTRACT

BACKGROUND:Cytokines secreted from neurons and glial cel s in early stage of spinal cord injury probably are essential factors for inducing secondary immunologic injury. OBJECTIVE:To investigate the effects of interleukin-1β, interleukin-6 and interleukin-17 on inflammatory reaction after acute spinal cord injury. METHODS:A total of 75 adult male Sprague-Dawley rats were randomly divided into control group and the spinal cord injury groups1, 6, 24 and 72 hours. A rat model of incomplete spinal cord injury was established by the modified Al en weight drop method. The control group just underwent laminectomy. Injured spinal cord and spleen tissues were col ected at corresponding time points after model induction. Immunohistochemical staining was used to detect the distribution and expressions of interleukin-6 and interleukin-17 in spinal cord tissue. Western blot assay was utilized to detect the changes in p-STAT3 expression in injured spinal cord. RT-PCR was applied to measure the mRNA expression of interleukin-1β, interleukin-6 and interleukin-17 in the spleen. RESULTS AND CONCLUSION:The expression levels of p-STAT3, interleukin-1β, interleukin-6, and interleukin-17 were significantly higher in the spinal cord injury groups than those in the control group (P<0.05). The expression of inflammatory cytokines increased immediately after injury. Interleukin-1βand interleukin-6 levels peaked at 6 hours, and then decreased. p-STAT3 and interleukin-17 levels peaked at 24 hours, and then decreased. The expression was stil higher at 72 hours than that in the control group. Results suggested that the expression of p-STAT3-mediated pro-inflammatory cytokines interleukin-1βand interleukin-6 in early stage increased. Inflammatory cascade would enlarge in the injured area, which probably induced secondary spinal cord injury and increased interleukin-17 levels. These possibly played a key role in secondary inflammatory reaction.