급성 척수손상시 세포사망의 특성

Abstract

OBJECTIVE: In acute spinal cord injury, biomechanical and pathological changes in the cord may worsen after injury. To explain these phenomena, the concept of the secondary injury has evolved and numerous pathophysiological mechanisms have postulated. These, however, have mainly focused only on the cell necrosis. The aim of present study is to verify whether apoptosis plays a role in the animal model of secondary injury of spinal cord. MATERIALS AND METHODS: Adult male Sprague-Dawley rats were laminectomized and spinal cord injury was induced using NYU spinal impactor at T9 segment. The animals were sacrificed periodically and tissue specimen was obtained at the injury segment, adjacent segments, and remote segments to observe the secondary injury ultimately for the observation of the spatial and temporal distribution and the related cells for the appearance of apoptosis, if present. RESULTS: In the spatial distribution of apoptosis, the apoptotic cells were located at gray matter of spinal cord and the number of apoptotic cells were significantly higher in adjacent segments than in the injured segment. In the temporal distribution of apoptosis, the number of apoptotic cells were maximal at 4 hours after injury and decreased subsequently. No apoptotic cells were found at remote segments which implies that there were no influence of apoptosis on transneuronal degeneration. CONCLUSION: These results suggest that the lesioned area of spinal cord expanded over time in acute spinal cord injury and apoptosis contributed to the spinal cord neuronal and glial cell loss. In conclusion, apoptosis is thought to have an important role in secondary injury of acute spinal cord injury.