Transplantation of viable mitochondria attenuates neurologic injury after spinal cord ischemia

ObjectivesSpinal cord ischemia (SCI) is one of the major concerns postoperative paraplegia during vascular or aortic surgery. Since mitochondrial dysfunction develops at early stage SCI, this study tested neuronal protective effect transplantation viable mitochondria to ischemic in rats.MethodsSCI was induced by crossclamping thoracic aorta T6 level for 25 minutes, followed release clip restore blood flow anesthetized rats. Mitochondria (100 ?g) were isolated from freshly harvested soleus muscle and delivered via internal jugular vein before releasing clip. The motor function assessed independently up 7 days after reperfusion. Spinal cords analyzed molecular histological changes.ResultsWhole-body vivo images acquired an imaging system confirmed enhancement MitoTracker fluorescence regions below cord. Compared with control vehicles, significantly improved lower-limb locomotor rats subjected Mitochondrial suppressed regional endoplasmic reticulum stress attenuating CCAAT-enhancer-binding protein homologous expression restoring binding immunoglobulin levels. In accordance, tissue levels interleukin-6, tumor necrosis factor-?, caspase-3 attenuated transplanted group. Histologic examination also showed significant increase numbers Nissls bodies neurons ventral horn following transplantation.ConclusionsOur that spinal ischemia–reperfusion injury oxidative injured cord, thereby reducing neuroapoptosis improving SCI.