Abstract:

BACKGROUND: Studies have demonstrated that tetrandrine has protection on acute spinal cord injury, but the specific mechanism remains poorly understood.
OBJECTIVE: To study the protection of tetrandrine on rat acute spinal cord injury and to study its mechanism from apoptosis pathway.
METHODS: A total of 100 rats were randomly divided into 4 groups. All rats were prepared for spinal cord injury models using modified Allen method except that in the sham-surgery group. Methylprednisolone and tetrandrine was injected into rats in the methylprednisolone and tetrandrine groups by tail intravenous injection prior to and at 24, 48 hours after model preparation. The same volume of physiological saline was injected in the sham-surgery and model groups. Basso-Beattie-Bresnahan (BBB score) was recorded at 8 hours, 1, 3, 7 and 14 days after model preparation. The morphological changes of spinal cord injury sites were observed by hematoxylin-eosin staining and the expressions of bcl-2 and bax were determined by immunohistochemistry.
RESULTS AND CONCLUSION: The BBB score of methylprednisolone and tetrandrine groups were significantly higher than that model group at 7 and 14 days (P < 0.05), but there were no significant difference between the methylprednisolone group and tetrandrine group (P > 0.05). Hematoxylin-eosin staining showed that the spinal cord injured severely at 3-7 days, the injury degree in the methylprednisolone group and tetrandrine group was slighter than that of the model group, with smaller bax expression and greater bcl-2 expression (P < 0.01). The findings demonstrated that, tetrandrine is able to protect neurons from apoptosis and promote the nerve function recovery by inhibiting the expression of Bax and promoting the expression of Bcl-2. Its effect is not inferior to methylprednisolone.