Abstract
To explore the effects of cervical sympathetic block (CSB) on facial nerve regeneration in rats and seek the optimal timing of treatment. A total of 72 adult Sprague-Dawley rats were divided randomly into 4 groups of sham-operation (sham), model control (NS), CSB1 and CSB2 (n = 18 each). Except for sham group, the model of peripheral facial paralysis was established for three other groups. After treating facial nerves injury with CSB at different timepoints, the behavioral changes of rats were observed.Electroneurography (ENoG) of injured nerves was performed and the expressions of glial cell derived neurotrophic factor (GDNF) of facial nerve nucleus were detected at different stages. The facial whisker movement function scores in sham, NS, CSB1 and CSB2 groups were 3.87 ± 0.35, 0.50 ± 0.52, 1.07 ± 0.62 and 0.81 ± 0.42 (F = 2.934, P = 0.035) at Day 7, 3.85 ± 0.37, 0.91 ± 0.52, 1.57 ± 0.65 and 1.07 ± 0.62 (F = 2.537, P = 0.038) at Day 14 and 3.85 ± 0.37, 1.71 ± 0.47, 3.00 ± 0.68 and 2.36 ± 0.49 (F = 3.627, P = 0.024) at Day 28. At Day 7, LatSD and AmpSD were not detected in NS, CSB1 and CSB2 groups.However, at Day 14, the values of LatSD were (1.26 ± 0.19), (6.67 ± 0.36), (4.67 ± 0.36) and (6.17 ± 0.36) ms, showing a significant difference (F = 3.052, P = 0.024) and AmpSD (6.42 ± 1.93), (2.16 ± 1.87), (4.16 ± 1.80) and (3.66 ± 1.40) mv, also a significance (F = 3.634, P = 0.021). And at Day 28, LatSD were (1.31 ± 0.17), (3.17 ± 0.19), (1.93 ± 0.12) and (2.60 ± 0.22) ms (F = 2.729, P = 0.032) and AmpSD (6.82 ± 2.30), (4.72 ± 5.23), (6.22 ± 3.50) and (5.82 ± 4.10) mv (F = 3.827, P = 0.019). The expression quantities of GDNF in 4 groups produced significant differences at Day 7 (4.67 ± 0.81, 13.52 ± 0.58, 26.17 ± 1.01 and 14.86 ± 1.03, F = 3.637, P = 0.028), Day 14 (5.67 ± 0.57, 24.41 ± 2.86, 26.52 ± 1.36 and 25.48 ± 1.42, F = 2.946, P = 0.031) and Day 28 (5.37 ± 0.92, 26.64 ± 1.68, 27.38 ± 1.66 and 25.69 ± 1.99, F = 4.273, P = 0.012). During early stage of facial nerve injury, the treatment of CSB may increase the expression of GDNF of facial nerve nucleus at early stage and thus accelerate the recovery of facial nerve injury in rats.
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