International journal of cardiology · 2007
Activation of interleukin-1 beta (IL-1 beta) signaling in the spinal cord in the rats with experimental cardiac injury.
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Xu Jun-Mei, Tao Li-Jian, Fu Di, Lv Zhi-Ping, Li Li, Dai Ru-Ping
Аннотация
BACKGROUND: The involvement of central nervous system (CNS) interleukin-1 beta (IL-1 beta) 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-1 beta 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-1 beta was upregulated in the upper thoracic spinal cord following cardiac injury. The upregulated IL-1 beta was distributed in the dorsal and ventral horns in the thoracic spinal cord as determined by immunohistochemistry. In situ hybridization demonstrated that IL-1 beta mRNA localized in the neurons was elevated in response to cardiac injury. The DNA binding activities of two IL-1 beta transcription factors, activator protein (AP)-1 and nuclear factor kappa B (NF-kappaB), were enhanced after cardiac injury. In correlated with the upregulation of the spinal IL-1 beta, the circulating IL-1 beta level was also increased following cardiac injury.
CONCLUSIONS: Acute cardiac injury could activate the spinal IL-1 beta signaling, which, in turn, may contribute to disease progression in the acute phase of cardiac injury in clinical practice.
METHODS AND RESULTS: Cardiac injury model in rats was established by intra-myocardial injection of formalin through the diaphragm. Western blot showed that IL-1 beta was upregulated in the upper thoracic spinal cord following cardiac injury. The upregulated IL-1 beta was distributed in the dorsal and ventral horns in the thoracic spinal cord as determined by immunohistochemistry. In situ hybridization demonstrated that IL-1 beta mRNA localized in the neurons was elevated in response to cardiac injury. The DNA binding activities of two IL-1 beta transcription factors, activator protein (AP)-1 and nuclear factor kappa B (NF-kappaB), were enhanced after cardiac injury. In correlated with the upregulation of the spinal IL-1 beta, the circulating IL-1 beta level was also increased following cardiac injury.
CONCLUSIONS: Acute cardiac injury could activate the spinal IL-1 beta signaling, which, in turn, may contribute to disease progression in the acute phase of cardiac injury in clinical practice.