K Yu1, X Ye, S Qu. 1. Department of Orthopedics, Changzheng Hospital, Second Military Medical University, Shanghai 201103, China.
Abstract
OBJECTIVE: To observe the value of gene therapy to spinal cord injury in vivo by transferring gene of brain-derived neurotrophic factor (BDNF) to rat myoblast with retroviral vector electrophysiologically. METHODS: Transection of spinal cord at the level of T9 was produced in 30 adult SD rats that were divided randomly into three groups: BDNF gene modified myoblast implantation (group A), myoblast implantation (group B), and no cell implantation as controls (group C). Three months after operation, whether the axon had regenerated and how the neural function was restored were observed, using the techniques of cerebral somatosensory evoked potential (CSEP) and motor evoked potential (MEP). RESULTS: Three months after injury, 3 rats in group A showed CSEP signals and 5 rats MEP signals, but no electrophysiological response was found in group B or group C. The amplitudes of the recovery of CSEP or MEP signals decreased and their latencies increased as compared with those before injury. The neural function of the spinal cord was greater in group A than in B and C. CONCLUSION: Treatment with genetically modified myoblasts producing BDNF can accelerate recovery from traumatic spinal cord injury in adult rats.
OBJECTIVE: To observe the value of gene therapy to spinal cord injury in vivo by transferring gene of brain-derived neurotrophic factor (BDNF) to rat myoblast with retroviral vector electrophysiologically. METHODS: Transection of spinal cord at the level of T9 was produced in 30 adult SD rats that were divided randomly into three groups: BDNF gene modified myoblast implantation (group A), myoblast implantation (group B), and no cell implantation as controls (group C). Three months after operation, whether the axon had regenerated and how the neural function was restored were observed, using the techniques of cerebral somatosensory evoked potential (CSEP) and motor evoked potential (MEP). RESULTS: Three months after injury, 3 rats in group A showed CSEP signals and 5 rats MEP signals, but no electrophysiological response was found in group B or group C. The amplitudes of the recovery of CSEP or MEP signals decreased and their latencies increased as compared with those before injury. The neural function of the spinal cord was greater in group A than in B and C. CONCLUSION: Treatment with genetically modified myoblasts producing BDNF can accelerate recovery from traumatic spinal cord injury in adult rats.