Activation of interleukin-1beta (IL-1β) signaling in the spinal cord in the rats with experimental cardiac injury

Background The involvement of central nervous system (CNS) interleukin-1beta (IL-1β) in the pathogenesis of acute cardiac injury is still an unexplored issue. The present study was aimed to investigate whether cardiac injury could induce the activation of IL-1β in the spinal cord. Methods and results Cardiac injury model in rats was established by intra-myocardial injection of formalin through the diaphragm. Western blot showed that IL-1β was upregulated in the upper thoracic spinal cord following cardiac injury. The upregulated IL-1β was distributed in the dorsal and ventral horns in the thoracic spinal cord as determined by immunohistochemistry. In situ hybridization demonstrated that IL-1β mRNA localized in the neurons was elevated in response to cardiac injury. The DNA binding activities of two IL-1β transcription factors, activator protein (AP)-1 and nuclear factor kappa B (NF-κB), were enhanced after cardiac injury. In correlated with the upregulation of the spinal IL-1β, the circulating IL-1β level was also increased following cardiac injury. Conclusions Acute cardiac injury could activate the spinal IL-1β signaling, which, in turn, may contribute to disease progression in the acute phase of cardiac injury in clinical practice.