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脊髓损伤后硫酸软骨素蛋白多糖及GFAP表达的变化*
The expression of chondroitin sulfate proteoglycan and GFAP after spinal cord injury
  
DOI:
中文关键词:  脊髓损伤  硫酸软骨素蛋白多糖  胶质纤维酸性蛋白
英文关键词:Spinal cord injury  Chondroitin sulfate proteoglycan  Glial fibrillary acidic protein
基金项目:
作者单位
王国毓 程志坚 杨保辉 李浩鹏 贺西京  
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中文摘要:
      目的 探讨脊髓损伤后NG2、Neurocan、GFAP表达的变化。方法 将32只雌性SD大鼠随机分为空白对照组和模型组。模型组采用脊髓横切法制作脊髓损伤模型,空白对照组仅切除T10全椎板及T9、T11部分椎板,对脊髓未作任何处理。分别在大鼠脊髓损伤制作后3、7、14及28 d时取材,利用免疫组织化学染色方法检测NG2、Neurocan、GFAP的表达情况。结果 模型组脊髓损伤后3 d时NG2的表达出现明显升高,7 d时NG2的表达达到最高点,14 d及28 d时NG2仍然维持在较高水平,但与7 d时的表达相比有下降,空白对照组NG2各时间点均呈低表达。模型组脊髓损伤后7 d时Neurocan的表达显著增加,于14 d时达到最高点,从14 d开始Neurocan的表达开始逐步下降,空白对照组Neurocan各时间点均呈低表达。模型组脊髓损伤后3 d时GFAP的表达明显升高,14 d时GFAP的表达达到顶点,28 d时损伤部位GFAP的表达均较空白对照组明显升高,两组比较差异有统计学意义(均P<0.05)。结论 脊髓损伤后NG2、Neurocan、GFAP表达升高,可能是脊髓损伤后抑制轴突再生的因素之一。
英文摘要:
      Objective To investigate the expression of NG2, Neurocan and glial fibrillary acidic protein(GFAP) after spinal cord injury. Methods Thirty-two female SD rats were randomly divided into two groups, namely blank control group and model group. In the blank control group, only T10 total lamina and T9 and T11 partial lamina were incised, and no further treatment was performed on the spinal cord. Spinal cord transection was used to model spinal cord injury in the model group. The expressions of NG2, Neurocan and GFAP were detected by immunohistochemical staining at 3, 7, 14 and 28 days after spinal cord injury. Results NG2 was low in the blank control group at each time point. In the model group, the expression of NG2 was significantly increased 3 days after spinal cord injury, and reached its peak at 7 days. At 14 and 28 days, the expression of NG2 was still at a high level, but slightly decreased compared with that at 7 days. The expression of Neurocan was lower in the blank control group at all time points. Neurocan expression was significantly increased 3 to 7 days after spinal cord injury in the model group and reached its peak at 14 days. The expression of Neurocan began to decrease gradually from 14 days after spinal cord injury. The expression of GFAP at 3, 7, 14 and 28 days in the model group was significantly higher than that in the blank control group (all P<0.05, with statistical difference). In the model group, GFAP expression was significantly increased 3 days after spinal cord injury, and reached its peak at 14 days. Conclusion Increased expression of NG2, Neurocan and GFAP after spinal cord injury may be part of the mechanisms that inhibit axonal regeneration.
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