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目的 :探讨bFGF是否对脊髓损伤后的大脑皮质运动神经元具有保护作用。方法 :用Nissl染色和GFAP免疫染色对脊髓半离断后的大脑皮质运动区神经元和胶质细胞进行了定量和定性研究。结果 :1 Nissl染色显示 :( 1)在对照组大鼠额皮质内神经元和神经胶质细胞未见异常 ;( 2 )在损伤组大鼠额皮质内见到大量神经元变性和胶质细胞增生明显以及胶质细胞嗜神经元现象 ;( 3 )在治疗组大鼠额皮质区内未见嗜神经元现象 ,但胶质细胞增生仍较明显。 2 GFAP免疫染色显示 :( 1)在对照组大鼠额皮质内见GFAP免疫阳性的星形胶质细胞主要分布 1、2层和胼胝体内 ;( 2 )在损伤组大鼠额皮质和胼胝体内见到大量增生的星形胶质细胞 ;( 3 )在治疗组大鼠额皮质和胼胝体内星形胶质细胞的形态和分布与对损伤组的一致。 3 GFAP免疫阳性细胞的统计显示 ,三组大鼠额皮质和胼胝体内GFAP免疫阳性细胞数为损伤组 >治疗组 >对照组的趋势 ,但损伤组与治疗组的数量差异无显著性 (P >0 .0 5 )。结论 :据上述结果 ,作者认为在脊髓半离断后外源性bFGF在功能上代替了部分损伤后引致大脑皮质内增生的星形胶质细胞分泌的内源bFGF ,两者共同对大脑皮质运动神经元产生保护性作用 ,即外源性bFGF对脊髓损伤的继发性脑病变有治疗作用。
Objective: To investigate whether bFGF can protect cortical motor neurons after spinal cord injury. Methods: Nissl staining and GFAP immunostaining were used to quantitatively and qualitatively study neurons and glial cells in the motor cortex of the spinal cord after semi-severed spinal cord. Results: 1 Nissl staining showed: (1) no abnormalities were found in the frontal cortex neurons and glial cells in the control group; (2) a large number of neuron degeneration and glial cells were seen in the frontal cortex Hyperplasia and glial cell neuron phenomenon. (3) There was no neurotropic phenomenon in the frontal cortex in the treatment group, but glial cell proliferation was still more obvious. 2 GFAP immunostaining showed that: (1) GFAP immunopositive astrocytes in the frontal cortex of rats in the control group were mainly distributed in the first and second layers and in the corpus callosum; (2) In the frontal cortex and the corpus callosum See a large number of hyperplastic astrocytes; (3) in the treatment group, frontal cortex and corpus callosum astrocytes in the shape and distribution of the same injury group. The statistics of GFAP immunopositive cells showed that the number of GFAP positive cells in the frontal cortex and the corpus callosum in the three groups was the trend of injury group> treatment group> control group, but there was no significant difference between the injury group and the treatment group (P> 0 .0 5). CONCLUSION: Based on the above results, the authors suggest that exogenous bFGF functionally replaces endogenous bFGF secreted by astrocytes that cause hyperplasia in the cerebral cortex after partial spinal cord transection, both of which contribute to cerebral cortical motor neurons Meta-producing protective effect of exogenous bFGF on spinal cord injury secondary brain lesions have a therapeutic effect.