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Updated: Sep 12, 2026

Protocol for Culturing Sympathetic Neurons from Rat Superior Cervical Ganglia (SCG)
Published on: January 29, 2009
Effect of nerve growth factor on neuronal apoptosis after spinal cord injury in rats
Xiaojian Cao1, Changhua Tang, Yongxiang Luo
1Department of Orthopaedics, First Affiliated Hospital, Nanjing Medical Universit y, Nanjing 210029, China. jsphkjc@sina.com
Objective:
To explore the molecular mechanism of the protective effect of nerve growth factor (NGF) on injured spinal cord.
Methods:
The posterior T(8) (the 8th thoracic segment) spinal cords of 60 Wistar rats were injured by impacts caused by objects (weighing 10 g) falling from a height of 2.5 cm with Allen's way. Solution with nerve growth factors (NGF) was given to 30 rats (the NGF group) through a microtubule inserted into the subarachnoid cavity immediately, and at 2, 4, 8, 12 and 24 hours after spinal cord injury (SCI) respectively. Normal saline (NS) with same volume was given to the other 30 rats (the NS group) with the same method. And 5 normal rats were taken as the normal controls. The expression of bcl-2 and bax proteins in spinal cord was detected with immunohistochemistry. The apoptotic neurons in spinal cord were measured with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling of DNA fragments (TUNEL) staining.
Results:
The positive expression of bcl-2 protein was strong in the normal controls, but decreased in the NS group, and increased significantly in the NGF group as compared with that of the NS group (P<0.01). The positive expression of bax protein was also strong in the normal controls, but increased in the NS group, and decreased significantly in the NGF group as compared with that of the NS group (P<0.01). Apoptotic neurons were found in the NS group, and they decreased significantly in the NGF group as compared with that of the NS group (P<0.01).
Conclusions:
NGF can protect the injured nerve tissues through stimulating the expression of bcl-2 protein, inhibiting the expression of bax protein and inhibiting the neuronal apoptosis after SCI.
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