title: Sodium hyaluronate-CNTF gelatinous particles promote axonal growth, neurogenesis and functional recovery after spinal cord injury.
abstract: OBJECTIVE
  Currently, effective therapeutic strategy for spinal cord injury (SCI) is not clinically available. To establish a better method that may help repair the injured spinal cord, sodium hyaluronate-ciliary neurotrophic factor (CNTF) gelatinous particles were generated.
  
  
  METHODS
  A segment of spinal cord tissue was excised to form a 2.5-mm-long cavity at thoracic level in an adult rat, and sodium hyaluronate-CNTF gelatinous particles were implanted into the lesion cavity. The recovery of the injured spinal cord was evaluated by immunohistochemistry, nerve tracing, electrophysiological test and Basso-Beattie-Bresnahan locomotor rating scale.
  
  
  RESULTS
  Open-field locomotion of the sodium hyaluronate-CNTF rats was significantly enhanced up to 12 weeks postoperation. Together with the evidence of enhanced cortical motor evoked potentials and cortical somatosensory evoked potentials in the sodium hyaluronate-CNTF group, these findings suggested a powerful functional recovery component. Immunohistochemical analyses suggested that the functional recovery might be attributable partly to an increase in axonal regrowth as well as in replenishment of β-tubulin-III-positive neuron-like cells.
  
  
  CONCLUSIONS
  Sodium hyaluronate-CNTF gelatinous particles may provide an effective method for treating SCI.
authors.affiliation: Department of Neurobiology and Beijing Institute for Neuroscience, Capital Medical University, Beijing, China.
authors.forename: N
authors.initials: N
authors.lastname: Wang
authors.affiliation: China National Center of Biomedical Analysis, Beijing, China.
authors.forename: S
authors.initials: S
authors.lastname: Zhang
authors.affiliation: Beijing Friendship Hospital, Capital Medical University, Beijing, China.
authors.forename: A F
authors.initials: AF
authors.lastname: Zhang
authors.affiliation: Department of Neurobiology and Beijing Institute for Neuroscience, Capital Medical University, Beijing, China.
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Yang
authors.affiliation: Department of Neurobiology and Beijing Institute for Neuroscience, Capital Medical University, Beijing, China.
authors.forename: X G
authors.initials: XG
authors.lastname: Li
mesh_terms: D000818:Animals; D001369:Axons / Q000187:drug effects / Q000502:physiology; D049108:Cell Enlargement / Q000187:drug effects; D020934:Ciliary Neurotrophic Factor / Q000008:administration & dosage*; D003692:Delayed-Action Preparations; D004195:Disease Models, Animal; D004337:Drug Carriers; D019054:Evoked Potentials, Motor / Q000187:drug effects; D005073:Evoked Potentials, Somatosensory / Q000187:drug effects; D005260:Female; D006820:Hyaluronic Acid / Q000008:administration & dosage*; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D055495:Neurogenesis / Q000187:drug effects / Q000502:physiology; D018696:Neuroprotective Agents / Q000008:administration & dosage*; D011897:Random Allocation; D017208:Rats, Wistar; D020127:Recovery of Function / Q000187:drug effects / Q000502:physiology; D013116:Spinal Cord / Q000187:drug effects / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000503:physiopathology; D013904:Thoracic Vertebrae; D054457:Tissue Scaffolds; D014404:Tubulin / Q000378:metabolism
chemical_list: D020934:Ciliary Neurotrophic Factor; D003692:Delayed-Action Preparations; D004337:Drug Carriers; D018696:Neuroprotective Agents; C488416:Tubb3 protein, rat; D014404:Tubulin; D006820:Hyaluronic Acid