The present study was undertaken to examine the effects of methylprednisolone on the expression and activity of calpain in spinal cord tissue following spinal cord ischemia-reperfusion injury in rats. Adult male Sprag...The present study was undertaken to examine the effects of methylprednisolone on the expression and activity of calpain in spinal cord tissue following spinal cord ischemia-reperfusion injury in rats. Adult male Sprague-Dawley rats were subjected to sham operations, ischemia-reperfusion and vehicle treated, or ischemia-reperfusion with methylprednisolone administration after injury. The expression of calpain I in the injured segments of the spinal cord as well as the degradation of the 68 kD neurofilament protein (NFP), a calpain-specific substrate, was determined at 3 h, 24 h, 72 h and 7 days after reperfusion using immunohistochemical labeling and western blot analysis, respectively. Three hours after spinal cord reperfusion, calpain I-positive cells and NFP degradation products were evident. The number of positive cells and immunoreactivity increased with time and peaked at 72 h after reperfusion. In addition, the number of calpain I-positive cells and the abundance of NFP degradation products were significantly lower in the methylprednisolone group, compared with vehicle treated animals following ischemia-reperfusion injury. The results of this study suggest that methylprednisolone can inhibit the expression and degradation activity of calpain following ischemia-reperfusion injury, providing further insight into the therapeutic benefits of methylprednisolone treatment for spinal cord injury.展开更多
文摘The present study was undertaken to examine the effects of methylprednisolone on the expression and activity of calpain in spinal cord tissue following spinal cord ischemia-reperfusion injury in rats. Adult male Sprague-Dawley rats were subjected to sham operations, ischemia-reperfusion and vehicle treated, or ischemia-reperfusion with methylprednisolone administration after injury. The expression of calpain I in the injured segments of the spinal cord as well as the degradation of the 68 kD neurofilament protein (NFP), a calpain-specific substrate, was determined at 3 h, 24 h, 72 h and 7 days after reperfusion using immunohistochemical labeling and western blot analysis, respectively. Three hours after spinal cord reperfusion, calpain I-positive cells and NFP degradation products were evident. The number of positive cells and immunoreactivity increased with time and peaked at 72 h after reperfusion. In addition, the number of calpain I-positive cells and the abundance of NFP degradation products were significantly lower in the methylprednisolone group, compared with vehicle treated animals following ischemia-reperfusion injury. The results of this study suggest that methylprednisolone can inhibit the expression and degradation activity of calpain following ischemia-reperfusion injury, providing further insight into the therapeutic benefits of methylprednisolone treatment for spinal cord injury.
