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

1. The aim of the present study was to examine the effect of glucocorticoids on neuropathic pain using a rat spare nerve injury (SNI) model. 2. 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 mu g 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)-alpha and interleukin (IL)-1 beta levels in spinal cord tissue were quantified 1, 3, 7 and 14 days after SNI. 3. 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-alpha and IL-1 beta were significantly lower in the D1 and D2 groups compared with the S group at all time points after surgery (P < 0.05). 4. Betamethasone suppressed astrocyte activation and increases in TNF-alpha and IL-1 beta 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.