Corticosterone administration results in a significant decrease of IL6r and gp130, but not IL-6 protein in the rat dorsal root ganglia following sciatic nerve ligature
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| Year of publication | 2008 |
| Type | Conference abstract |
| MU Faculty or unit | |
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| Description | Interleukin-6 (IL-6) is proinflammatory cytokine that has been implicated in the development of neuropathic pain. It binds to specific receptor IL-6R and the IL-6/IL-6R complex is responsible for the homodimerization of the transmembranous signal transducer gp130. Many studies have shown that corticosterone administration effectively reduces the production of inflammatory mediators including cytokines. In the present study we detected an immunofluorescence (IF) for IL-6 and its receptors in the rat L4 dorsal root ganglion (DRG) cells of the naive rats and those following sciatic nerve ligature and corticosterone administrations. Naive DRG showed only low IF intensity for IL-6 and its receptors in the small- and medium-sized neurons and the satellite glial cells (SGC) surrounding large neurons. Sciatic nerve ligature induced an increased level of IF for IL-6, IL-6R, and gp130 in the small- and medium-sized neurons, and predominantly in the large neuron-SGC units from 3 to 14 days after surgery. While following corticosterone administration 3 and 6 days from operation IF intensity for IL-6 remained at similar level like in DRG without administration, IF intensity for IL-6R and gp130 was markedly decreased, and only a weak IF was found in the neurons. Our results showed that corticosterone administration did not result in expected robust decrease of IF for IL-6 in contrast to IL-6 receptors that mediate a biological effect of IL-6. |
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