OBJECTIVE: To observe the temporal changes of basic fibroblast growth factor (FGF-2) expression in the spinal cord of a rat model of spared nerve injury (SNI) of the sciatic nerve. METHODS: A total of 100 male SD rats were randomly divided into sham-operated group and SNI group. The paw withdrawal threshold to mechanical stimulation was recorded at 1 day before and at 1, 4, 7, 14 and 28 days after the operation. The expressions of FGF-2, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the L4-6 spinal cord segments of the rats were measured at the specified time points. RESULTS: The paw withdrawal threshold began to decline at 1 day after SNI, reached the lowest level at 7 days, and maintained a low level till 28 days (P<0.05). The expression of FGF-2 began to increase significantly on postoperative day 4, reached the peak level on day 14 and maintained the high level till day 28 (P<0.05). The rats with SNI showed significantly higher expressions of TNF-α and IL-6A in the spinal cord than those in the sham-operated group at each time point of measurement (P<0.05). CONCLUSIONS: SNI of the sciatic nerve can induce neuropathic tactile allodynia and causes up-regulation of FGF-2 and inflammatory cytokines in the spinal cord.
OBJECTIVE: To observe the temporal changes of basic fibroblast growth factor (FGF-2) expression in the spinal cord of a rat model of spared nerve injury (SNI) of the sciatic nerve. METHODS: A total of 100 male SD rats were randomly divided into sham-operated group and SNI group. The paw withdrawal threshold to mechanical stimulation was recorded at 1 day before and at 1, 4, 7, 14 and 28 days after the operation. The expressions of FGF-2, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the L4-6 spinal cord segments of the rats were measured at the specified time points. RESULTS: The paw withdrawal threshold began to decline at 1 day after SNI, reached the lowest level at 7 days, and maintained a low level till 28 days (P<0.05). The expression of FGF-2 began to increase significantly on postoperative day 4, reached the peak level on day 14 and maintained the high level till day 28 (P<0.05). The rats with SNI showed significantly higher expressions of TNF-α and IL-6A in the spinal cord than those in the sham-operated group at each time point of measurement (P<0.05). CONCLUSIONS: SNI of the sciatic nerve can induce neuropathic tactile allodynia and causes up-regulation of FGF-2 and inflammatory cytokines in the spinal cord.