Objective: To investigate the effect of acute cardiac injury on the activation of interleukin-1 beta (IL-1 beta) signaling in the spinal cord.
Methods: Acute cardiac injury rat model was established by intra-myocardial injection of formalin through diaphragm. IL-1 beta expression was determined by Western blot, immunohistochemistry and in situ hybridization. The DNA binding activities of 2 IL-1 beta transcription factors, activator protein (AP)-1 and nuclear factor kB (NF-kappaB) were measured by electrophoretic mobility shift assay (EMSA).
Results: After cardiac injury, the IL-1 beta protein level was dramatically upregulated in the spinal cord. The upregulated IL-1 beta was mainly expressed in the neurons in the lamina II approximately IV of the spinal cord. In response to cardiac injury, the DNA binding activities of NF-kappaB and AP-1 were greatly activated.
Conclusion: Acute cardiac injury could activate the spinal IL-1 beta signaling, which, in turn, may be involved in the progression of heart failure after injury.