Effects of betamethasone on neuropathic pain in a rat spare nerve injury model

SUMMARY The aim of the present study was to examine the effect of glucocorticoids on neuropathic pain using a rat spare nerve injury ( SNI ) model. Eighty rats were treated divided into the following groups: (i) a sham‐operated group; (ii) a group subjected to SNI (S); (iii) a group subjected to SNI and administered 4 μg betamethasone intrathecally (D1); and (iv) a group subjected to SNI and administered 1 mg betamethasone at the site of nerve injury (D2). The mechanical withdrawal threshold ( MWT ) and thermal withdrawal duration ( TWD ) were measured 1 day before and the 1, 3, 7 and 14 days after SNI . Glial fibrillary acidic protein, glucocorticoid receptor ( GR ), tumour necrosis factor ( TNF )‐α and interleukin ( IL )‐1β levels in spinal cord tissue were quantified 1, 3, 7 and 14 days after SNI . The MWT was significantly higher in the D2 compared with S group 3–14 days after surgery and compared with the D1 group 7 and 14 days after surgery ( P < 0.05). The TWD was significantly lower in the D2 group compared with the S and D2 groups 3–14 days after surgery ( P < 0.05). Glial fibrillary acidic protein expression was significantly lower in the D1 and D2 groups compared with the S group 3–14 days after surgery ( P < 0.05). Glucocorticoid receptor expression was significantly higher in the D1 group compared with the S and D2 groups after surgery ( P < 0.05). Levels of TNF ‐α and IL ‐1β were significantly lower in the D1 and D2 groups compared with the S group at all time points after surgery ( P < 0.05). Betamethasone suppressed astrocyte activation and increases in TNF ‐α and IL ‐1β levels in a rat model of neuropathic pain. Local injection of betamethasone resulted in smaller increases in spinal GR expression and more pronounced improvement in pain behaviour compared with intrathecal injection.