Sharma H S, Westman J, Gordh T, Alm P
Laboratory of Neuroanatomy, Department of Medical Cell Biology, Biomedical Centre, Uppsala University, Uppsala, Sweden.
Acta Neurochir Suppl. 2000;76:365-9. doi: 10.1007/978-3-7091-6346-7_76.
Influence of brain derived neurotrophic factor (BDNF) on carbon monoxide (CO) production following spinal cord injury was examined using expression of the constitutive isoform of the enzyme hemeoxygenase-2 (HO-2) in a rat model. A longitudinal incision of the right dorsal horn on the T10-11 segment markedly increased the HO-2 immunostaining in the cord at 5 h. At this time period, breakdown of the blood-spinal cord barrier (BSCB) and edema formation were quite prominent. Repeated topical application of BDNF (20 microliters of a 1 microgram/ml solution) over the exposed surface of the cord significantly attenuated the edematous expansion of the cord and the disturbances in the BSCB permeability. In BDNF-treated rats, expression of HO-2 immunoreactivity was considerably reduced. These results strongly suggest that BDNF is neuroprotective in spinal trauma and this growth factor has the capacity to attenuate CO production by downregulating HO-2 expression.
利用大鼠模型中血红素加氧酶-2(HO-2)组成型同工型的表达,研究了脑源性神经营养因子(BDNF)对脊髓损伤后一氧化碳(CO)产生的影响。在T10-11节段右背角做纵向切口,5小时时脊髓中HO-2免疫染色显著增加。在此时间段,血脊髓屏障(BSCB)破坏和水肿形成相当明显。在脊髓暴露表面反复局部应用BDNF(20微升1微克/毫升溶液)可显著减轻脊髓的水肿扩张和BSCB通透性紊乱。在BDNF处理的大鼠中,HO-2免疫反应性表达明显降低。这些结果强烈表明,BDNF在脊髓创伤中具有神经保护作用,并且这种生长因子有能力通过下调HO-2表达来减弱CO的产生。