Somatostatin Type 2 Receptor Antibody Enhances Mechanical Hyperalgesia in the Dorsal Root Ganglion Neurons after Sciatic Nerve-pinch Injury: Evidence of Behavioral Studies and Bax Protein Expression.

BACKGROUND:Our previous study has indicated that somatostatin potently inhibits neuropathic pain through the activation of its type 2 receptor 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 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 antibody (anti- 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 duanyu1942R2 antibody 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 treatment. CONCLUSION:The current data suggested that inhibitory changes in proteins from the apoptotic pathway in groups might be taking place to overcome the protein deficits caused by duanyu1942R2 antibody and supported the new therapeutic intervention with duanyu1942R2 antagonist for neuronal degeneration following nerve injury.

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