The expression and significance of Bcl-2，Ｂax following spinal cord injury induced by circle ligation after decompression at different time in rat

English Keywords:Spinal cord injury  Circle ligation    Ｄecompression  Apoptosis  Ｒａｔ

English Abstract:

  【Abstract】 Objective：To evaluate the neuron apoptosis and expression of Bcl-2 and Bax protein following spinal cord injury induced by circle ligation after decompression at different timepoint.Method：Eighty-four adult SD rats were divided randomly into four groups as following：group A，undergoing laminectomy and dural sac circumference measurements；group B undergoing decompression 8h later following ligation；group C undergoing decompression 72h later following ligation；group D undergoing ligation alone.Specimen of each group was harvested at 1 day，7　days，14 days and 21 days after surgery respectively.All specimenｓ were subjected to HE staining，Tunel staining and immunohistochemistry to evaluate the expression of Bax，Bcl-2 protein.The limb function was evaluated by using the BBB score.Result：Bax expression began to increase 1 day after decompression in group B and C，and reached peak at 7 days，while still remain visible 14 days after decompression，and then decreased at 21 days；group D increased gradually after surgery.Bcl-2 expression in group B and C increased continuously after decompression，while decreased continuously in group D.Under Tunel staining，apoptosis cells ｉｎ　ｇｒｏｕｐ　Ｂ，Ｃ　ａｎｄ　Ｄ　were evidenced 1 day after surgery，and reached peak 7 days later，then decreased，and still remained visible 21 days after surgery.Bcl-2/Bax ratio and number of Tunel positive cells showed negative association in group B and C，while positive in group D.BBB score in group A returned to normal 1 week after operation；while ｉｔ　increased continuously in group B and C；BBB score in group D decreased from 1 day after operation，and reached the lowest at 7 day，then increased gradully（P＞0.05）.Conclusion：Circle　ligation seems to establish the SCI model in rat，early decompression can decrease the secondary apoptosis and promote neurofunction recovery.