ABSTRACT
Transient receptor potential vanilloid 1 (TRPV1) is a non-selective cation channel, which can be activated by multiple pathways during the course of the diseases. Recent studies indicate that primary sensory neurons of the pancreas express TRPV1 receptor and the activation of TRPV1 receptor promotes pancreatic inflammation. Moreover, blockade of these transient receptor potential channels can greatly ameliorate the pain response in experimental pancreatitis.
ABSTRACT
Objective: To investigate the effect of edaravone on the pain sensitivity in rats with spinal nerve ligated and to probe into the related mechanism. Methods: Male adult SD rats were randomly divided into 3 groups: a sham (Sham) group, a spinal nerve ligation (SNL) group and edaravone(Eda) group. The paw withdrawal mechanical threshold(PWMT) was measured before and after ligation (once daily for 7 days). Rats were sacrificed at specified time points and the left(operation side) L4 and L5 dorsal root ganglia(DRG) and the right (control side) L5 DRG were obtained and immunostained to observe the changes of pJNK in DRG neurons and spinal cords, so as to observe the effect of edaravone on pJNK. Results: Edaravone can reduce the mechanical hyperalgesia induced by spinal nerve ligation. Immunostaining showed that the SNL group had an increased pJNK in the ipsilateral DRG neurons (L5) 24 hours after ligation; double immunofluorescence indicated that the expression of pJNK in the ipsilateral spinal astrocytes was increased 3 days after ligation. Edaravone can reduce pJNK expression in DRG neurons and spinal cords at corresponding time points. Conclusion: Edaravone can relieve the neuropathic pain induced by spinal nerve ligation, and the mechanism might be related to the inhibition of pJNK expression in DRG neurons and spinal cords.