Annexin A10 contributes to chronic constrictive injury-induced pain through activating ERK1/2 signalling in rats.

PURPOSE: The current study aims at investigating the downstream targets of spinal Annexin A10 in modulating neuropathic pain.

MATERIALS AND

METHODS

Paw withdrawal latency and paw withdrawal threshold were measured to evaluate the pain-associated behaviour in rats. The expression of spinal Annexin A10, phosphorylated-extracellular regulated kinase 1/2 and extracellular regulated kinase were detected by western blotting. The level of tumour necrosis factor-α and interleukine-1β was tested by enzyme-linked immunosorbent assay (ELISA) kits.

RESULTS

Chronic constrictive injury caused pain hypersensitivity in rats, along with increased expression of spinal Annexin A10, phosphorylated-extracellular regulated kinase 1/2, tumour necrosis factor-α and interleukine-1β in rats. Knockdown of spinal Annexin A10 suppressed the chronic constrictive injury-induced hyperalgesia, and inhibited the chronic constrictive injury-induced increased expression of phosphorylated-extracellular regulated kinase 1/2, tumour necrosis factor-α and interleukine-1β in the spinal cord. Inhibition of spinal extracellular regulated kinase activation decreased the release of tumour necrosis factor-α and interleukine-1β, but did not change the increased expression of Annexin A10 caused by chronic constrictive injury.

CONCLUSIONS

Annexin A10 contributed to the development of neuropathic pain by activating spinal extracellular regulated kinase signalling and the subsequent release of tumour necrosis factor-α and interleukine-1β in the spinal cord.