Background:
Our previous study has indicated that somatostatin potently inhibits neuropathic
pain through the activation of its type 2 receptor (SSTR2) in mouse dorsal root ganglion and
spinal cord. However, the underlying mechanism of this activation has not been elucidated clearly
Objective:
The aim of this study is to perform the pharmacological studies on the basis of sciatic
nerve-pinch mice model and explore the underlying mechanism involving SSTR2.
Methods:
On the basis of a sciatic nerve-pinch injury model, we aimed at comparing the painful behavior
and dorsal root ganglion neurons neurochemical changes after the SSTR2 antibody (anti-
SSTR2;5μl,1μg/ml) administration in the mouse.
Results:
After pinch nerve injury, we found that the mechanical hyperalgesia and severely painful behavior
(autotomy) were detected after the application of SSTR2 antibody (anti-SSTR2; 5μl, 1μg/ml)
on the pinch-injured nerve. The up-regulated phosphorylated ERK (p-ERK) expression and the apoptotic
marker (i.e., Bax) were significantly decreased in DRGs after anti-SSTR2 treatment.
Conclusion:
The current data suggested that inhibitory changes in proteins from the apoptotic pathway
in anti-SSTR2-treated groups might be taking place to overcome the protein deficits caused by
SSTR2 antibody and supported the new therapeutic intervention with SSTR2 antagonist for neuronal
degeneration following nerve injury.
Silencing the enhancer of zeste homologue 2, Ezh2, represses axon regeneration of dorsal root ganglion neurons
