ABSTRACT
Objective·To investigate the effects of sodium houttuyfonate (SH) on neurons in early traumatic spinal cord injury (TSCI) rats and its mechanism. Methods·Forty adult female rats were randomly divided into sham group (n=8), control group (n=8) and experimental group (n=24). The sham group only received opened laminectomy without spinal cord clamping, the spinal cords in other two groups were clamped. The experimental group was divided into low [0.06 g/(kg·d)], moderate [0.12 g/(kg·d)] and high [0.24 g/(kg·d)] dose subgroups, in which SH was administrated intragastrically 1 h after operation and next two days. The other groups were given equivalent normal saline. The best therapeutic dose of SH was screened out by the results of the BBB scores and Nissl staining. To explore the neuroprotection mechanisms of SH, 72 rats were randomly divided into sham group (n=24), model group (n=24) and SH best dose group (n=24), the postoperative interventions were as same as above. Immunofluorescence and immunohistochemistry were respectively used to detect the number of motor neurons and cleaved-caspase3 positive staining neurons, the expression of Bax, Bcl-2, NeuN and cleaved-caspase3 was detected by Western blotting. Results·The BBB scores on day 5 and day 7 after operation in low dose group were higher than those of control group (all P<0.01), but lower than those of moderate and high dose groups (all P<0.01), and the scores in the moderate and high dose groups were not different significantly. On day 7 after operation, compared with moderate and high dose groups, the dissolution of Nissl bodies in low dose group and control group increased, the number of Nissl bodies reduced, and the colour shallowed. But Nissl staining in moderate and high dose groups were similar. The optimal dose of SH was 0.12 g/(kg·d), which was judged by the results of BBB scores and Nissl staining. On day 3 and day 7 after operation, compared with control group, the number of motor neurons and the expression of NeuN and Bcl-2 in SH best dose group were increased (all P<0.01), while the number of cleaved-caspase3 positive staining neurons and the expression of Bax and cleaved-caspase3 were reduced (all P<0.01). Conclusion·SH has a certain neuroprotection on neurons in TSCI, its mechanism may be through upregulating the ratio of Bcl-2/Bax, thereby reducing the neuronal apoptosis.