Objective To evaluate the effect of sufentanil on apoptosis in spinal cord neurons of mice with peripheral nerve injury. Methods One hundred and fifty clean-grade healthy male BALB∕c mice, aged 6-8 weeks, weighing 18-22 g, were divided into 3 groups ( n=50 each) using a random number table method: sham operation group (group Sham), peripheral nerve injury group (group PNI) and sufentanil group ( group SF) . The model of unilateral sciatic nerve injury was established in PNI and SF groups. After establishing the model, sufentanil 5. 0 μg∕kg was intraperitoneally injected once a day for 3 consecutive days in group SF, while the equal volume of normal saline was given instead of sufentanil in Sham and PNI groups. Five mice in each group were sacrificed at days 1, 3, 7, 14 and 28 after surgery ( T0-4 ) , and L4-6 segments of the injure ipsilateral spinal cord were removed for examination of pathological changes ( with a light microscope) and for determination of neuronal apoptosis ( by TUNEL assay) . The ap-optosis index ( AI) was calculated. Five mice in each group were sacrificed at T0-4 , and L4-6 segments of the injured ipsilateral spinal cord were removed for detection of the expression of Bcl-2, Bax and cleaved caspase-3 by Western blot. The ratio of Bcl-2 expression to Bax expression ( Bcl-2∕Bax ratio) was calculat-ed. Results Compared with group Sham, the AI was significantly increased, the expression of Bcl-2 pro-tein was down-regulated, and the expression of cleaved caspase-3 and Bax was up-regulated in PNI and SF groups ( P<0. 05) . Compared with group PNI, the AI was significantly decreased, the expression of Bcl-2 protein was up-regulated, the expression of cleaved caspase-3 and Bax was down-regulated, the Bcl-2∕Bax ratio was increased (P<0. 05), and the pathological changes were significantly attenuated in group SF. Conclusion Sufentanil can inhibit apoptosis in spinal cord neurons of mice with peripheral nerve injury.

Objective To evaluate the effect of sufentanil on the expression of basic fibroblast growth factor(bFGF)in nerve tissues after peripheral nerve injury in mice. Methods One hundred pathogen-free healthy male Balb∕c mice, aged 6-8 weeks, weighing 18-22 g, were divided into 4 groups (n=25 each)using a random number table: peripherial nerve injury group(group PNI), high dose sufentanil group(group H), medium dose sufentanil group(group M)and low dose sufentanil group (group L). The model of unilateral sciatic nerve transaction was established in ketamine-anesthetized mice. Sufentanil 100, 50 and 25 μg∕kg were intraperitoneally injected immediately after establishment of the model once a day for 3 consecutive days in H, M and L groups, respectively. The equal volume of normal saline was given instead in group PNI. On 1, 2, 4, 8 and 12 weeks after establishment of the model, 5 mice were sacrificed and the nerve tissues were obtained from the site 05 cm up and down the lesion site of the nerve for examination of the shape of the myelin sheath of nerve fibers(with an electronic microscope).The expression of bFGF in the sciatic nerve tissue was detected by Western blot. Results The shape of medulla sheath was irregular, the thickness of myelin lamellae was thin, the separation of myelin lamellae was aggravate, demyelinate was found, and the proliferation of Schwann cells was not marked in group PNI. The shape of medulla sheath was regular, the thickness of myelin lamellae was dense, and the proliferation of Schwann cells was marked in group H. The shape of medulla sheath was irregular, the separation of mye-lin lamellae was observed, demyelinate was found, and the proliferation of Schwann cells was not marked in group L. Compared with group PNI, the expression of bFGF was significantly up-regulated in H, M and L groups(P<005). Compared with group L, the expression of bFGF was significantly up-regulated in H and M groups(P<005). Compared with group M, the expression of bFGF was significantly up-regulated in group H(P<005). Conclusion The mechanism by which sufentanil improves regeneration and repair after peripheral nerve injury may be related to up-regulating the expression of bFGF in nerve tissues of mice.

BALB/c mice were intraperitoneally injected with 10, 5 or 2.5 mg/kg Brazil for 14 days after sciatic nerve injury. Results demonstrate that the spleen T/B lymphocyte stimulation index and serum circulating immune complex concentration were significantly reduced, and the morphology of the soleus muscle was restored in mice with sciatic nerve injury. These effects of Brazil were dose-dependent. Our experimental findings indicate that Brazil can regulate immune responses after nerve injury and promote sciatic nerve repair.

Objective: The purpose of this study is to explore the immunosuppression of nuclear factor-kappa B (NF-kappa B) by intragastric brazilein in spinal cord segments connected with injured sciatic nerve in mice. Methods: Healthy adult BALB/c mice underwent unilateral sciatic nerve interruption and anastomosis and then were treated with physiological saline (blank group), high dose, middle dose and low dose of brazilein in separate groups. The potential amplitude and motor nerve conduction velocity (MNCV) were measured. Myelin was assayed by immunohistochemical staining. NF-kappa B levels were detected by Western blotting and real-time PCR. Results: The potential amplitude and MNCV in the high and middle dose groups were significantly higher than in the low dose group and blank group. Myelin of the high dose and middle dose groups had more integrity. NF-kappa B was activated in spinal cord L4-6 connected with injured sciatic nerve. During the survival time of 12 h, 24 h, 3 d, 5 d and 1 w, NF-kappa B expression of the high dose group and the middle dose group were significantly lower versus the low dose and bland groups (P < 0.05). Conclusion: Brazilein can inhibit the immune activation of NF-kappa B in neurons in spinal cord L4-6 connected with injured sciatic nerve, which promotes nerve regeneration.