| Purpose:Neuropathic pain (NP) is a consequence of injury or disease affecting the somatosensory system. NP threats the health of human seriously, however its mechanism is still unknown completely and there is no effective treatment. It is well known that there will be great changes of neuropeptides after injury in the dorsal root ganglion (DRG) and spinal dorsal horn (SDH), which causes NP. Neurotrophic peptide galanin (Gal) is strongly linked to several biological functions such as pain, development and trophic effects. A great deal of experimental data shows that Gal in DRG and SDH is upregulated in the state of nerve injury and play functions in antinociception, neurotrophy and neural regeneration. In this experiment, sciatic nerve-pinch injury rat model is used to study the functions of Gal and its receptors (GalR1, GalR2) in the state of nerve injury. It is wished to supply accurate and reliable theoretical basis for researches in neuropathic pain and clinical treatment for nerve injury. Materials and methods:Sixty-three rats catheterized successfully were randomly divided into3groups (21rats in each group). The first group is that rats with sciatic nerve-pinch injury were treated with vehicle solution. The second group is that rats with sciatic nerve-pinch injury were treated with Gal. The third group is that sham-operated control rats were just treated with vehicle solution. Then the threshold responses to mechanical and thermal stimuli were recorded everyday. Seven rats of each group were killed for tissue collection after NCV measurement at the day of8,16, and24(each time point7rats) after sciatic nerve-pinch injury. Real time-PCR and Western blot assay were used to analyze the levels of Gal, GalR1, and GalR2in L4-5DRG and the corresponding SDH. What is more, morphology of sciatic nerve was observed by toluidine blue staining and electron microscopy. Then the data were processed for statistical analysis. Results:(1) Exogenous Gal could release the NP in rats with sciatic nerve-pinch injury.(2) Gal increased significantly in DRG and SDH after sciatic nerve pinch injury. Gal administration downregulated Gal in DRG, but not SDH, after sciatic nerve pinch injury. GalR1decreased significantly in DRG after sciatic nerve pinch injury. Gal administration downregulated GalRl in DRG after sciatic nerve pinch injury as compared with that in sciatic nerve-pinched animals without Gal treatment. GalR1increased significantly in SDH after sciatic nerve pinch injury. Gal administration decreased GalR1in SDH after sciatic nerve pinch injury. GalR2increased significantly in DRG and SDH after sciatic nerve pinch injury. Gal administration did not have significant effects on GalR2expression in DRG and SDH after sciatic nerve pinch injury.(3) Exogenous Gal could improve sciatic NCV and nerve regeneration in rats with sciatic nerve-pinch injury. Conclusion:Gal and its receptor system take part in the pathophysiological processes of NP and nerve regeneration. In this model, by activating its receptors Gal release NP and promote nerve regeneration, which plays a protective role in nerve injury. These findings remind that it may be a potential way for curing NP to interfere Gal and its receptor system. |
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