ZHENG Liheng,LIN Hongsheng,LI Jincong.Effect of methylprednisolone on the neurocyte apoptosis following acute spinal cord injury[J].Chinese Journal of Spine and Spinal Cord,2012,(5):452-458.
Effect of methylprednisolone on the neurocyte apoptosis following acute spinal cord injury
Received:December 15, 2011  Revised:February 07, 2012
English Keywords:Spinal cord injury  Acute stage  Methylprednisolone  Apoptosis  TUNEL
Fund:澳门科学技术发展基金(026/2010/A);广东省科技计划项目(2010-170-1)
Author NameAffiliation
ZHENG Liheng Centro Hospitalar conde de Sao Januário, Macao, 9990781, China 
LIN Hongsheng 暨南大学骨科疾病研究所 
LI Jincong 澳门医学科技研究协会999078 澳门 
谢 林  
吴 昊  
张国威  
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English Abstract:
  【Abstract】 Objectives: To observe the effect of methylprednisolone on the spinal nerve cell apoptosis following acute spinal cord injury(ASCI) and investigate the mechanisms of spinal cord recovery. Methods: The spinal cord injury models were made according to Allen′s weight-drop method. All animals were divided randomly into 3 groups: sham group (group S, 36 rabbits), control group (group C, 36 rabbits) and treatment group (group T, 36 rabbits). Six rabbits were selected randomly and sacrificed, and the specimens were fixed with 4% paraformaldehyde at 8h, 24h, 72h, 7d, 14d and 28d after injury. Spinal cord motor nerve functions were evaluated by Rivlin loxotic plate scores and BBB Scoring system. The pathological changes among three groups were compared and analysed by HE staining and TUNEL test. Results: The loxotic plate critical angles and BBB scores after injury gradually increased in group C and T but remained unchanged in group S. The angles and scores of group T were higher than group C but lower than group S at each time-point in the following 7 days (P<0.05). No obvious changes were noted for HE staining in group S at different time points, spinal cord tissue lost its normal structure. Varying degrees of edema and neurocytes necrosis, vacuoles formation in gray matter, neutrophils and bleeding were noted in necrotic area in both group C and T. There were no significant differences between two groups at 8, 24 and 72 hours following SCI. Group T had better neurofunction recovery than group C at 7, 14 and 28 days. And group T had better recovered than group C at 7, 14, 28 days following SCI which presented with light degree of injury, gradually resolved haematoma, decreasing vacuole and gliocyte, resolving of gray and white matter and increasing of collagen fiber and neuron. Apoptotic cells were found in group C and T at 8 hours, which reached peak within 24 hours, maintained high level at 3 days, and decreased slowly at 7 days after injury, and the number of cells significantly decreased at 14 days and 28 days by TUNEL test, but no such findings were noted in group S during the whole period. At 8 hours, 24 hours, 3 days and 7 days, there were less apoptotic cells in group T than in group C (P<0.05). But no significant difference was found between group C and T at 14 and 28 days (P>0.05). Conclusions: Early use of methylprednisolone in acute SCI contributes to neurofunction recovery, which may be by means of anti-apoptosis.
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