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Objective: It has been widely acknowledged that early treadmill training plays an important role in rewiring neurons in a functionally meaningful manner in spinal cord injury (SCI) treatment. However, it is still unclear how early to start treadmill training to obtain the most efficacious results after SCI. The purpose of this study was to find the earliest time point when treadmill training was most effective in rewiring neurons., Methods: The rats were randomly divided into five groups: a sham group, control group, and three treadmill groups based on training start time post-injury: a 24 h group, 48 h group, and 72 h group., Results: The results revealed that in the 72 h group, Basso, Beattie, and Bresnaham scores increased and apoptotic cells decreased significantly compared to the other groups. There were no statistically differences in neuron counting and 5-bromo-2V-deoxyuridine assays between the groups., Conclusion: These results indicated that the best start time for treadmill training is 72 h after SCI.

After spinal cord injury (SCI), a series of complex pathophysiological processes follows the initial injury. Because inflammation plays a key role in this secondary pathology damage, anti-inflammatory drug treatment may reduce secondary damage and protect neurons after SCI. Though nordihydroguaiaretic acid (NDGA) can inhibit inflammatory responses, its potential roles in neuroprotection and anti- inflammation in an SCI model have not been studied. In this study, we investigated the anti-inflammatory effects of NDGA in SCI. First, histopathological alterations were evaluated with hematoxylin/eosin (HE) and Nissl staining, showing an increased number of neurons after NDGA administration. Additionally, the extent of secondary damage was assessed by TUNEL assay and measurement of astrocyte proliferation. The data showed that the numbers of apoptotic cells and the proliferative extent of astrocytes were significantly decreased by the use of NDGA. The anti-inflammatory effect of NDGA was evaluated by measuring myeloperoxidase (MPO) levels as an indicator of neutrophil activity, macrophage/microglia numbers, and expression of inflammatory cytokines including IL-1β and TNF-α. NDGA treatment significantly decreased the MPO level and the number of macrophages/microglia. In addition, NDGA also suppressed the expression of IL-1β and TNF-α after SCI. These data suggest that anti-inflammatory action by NDGA can reduce secondary damage after SCI., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Bridging strategies are essential for spinal cord repair in order to provide a physical substrate allowing axons to grow across the site of spinal cord lesions. In this study, we have evaluated the therapeutic effects of adding amniotic epithelial cells to a unidirectionally oriented acellular muscle scaffold and have compared this with the effect of a scaffold alone. Chemically extracted acellular muscles, with or without amniotic epithelial cells, were implanted into the lateral hemisected adult rat thoracic spinal cord. Control rats were similarly injured. After 4 weeks, the acellular muscle scaffolds were found to be well integrated with the host tissue. The chemically extracted acellular muscle scaffold seeded with amniotic epithelial cells promoted axonal growth in a distinctly organized and linear fashion, induced sprouting of calcitonin gene-related peptide positive axons, and was not associated with an astrocyte response. Compared with acellular muscle scaffolds alone, the addition of amniotic epithelial cells further promoted the remyelination of nerve fibers, sprouting of 5-hydroxytryptamine nerve fibers, relays of cortical motor-evoked potential and cortical somatosensory-evoked potential, and functional recovery. All these data together suggest that co-implantation of chemically extracted acellular muscle with amniotic epithelial cells may constitute a valuable approach to study and/or develop therapies for spinal cord injury., (Copyright © 2012 Wiley Periodicals, Inc.)

Extracellular matrix is the gold standard for tissue regeneration. In this study, we directly made the extracellular matrix of the tissue or organ into scaffold for spinal cord injuries, a strategy that is seldomly tried in spinal cord engineering. The aim of this study was to determine if the chemically extracted acellular muscle could be a potential scaffold for spinal cord injury. The chemically extracted acellular muscle was implanted in the lateral hemisected adult rat thoracic spinal cord. Control rats were similarly injured. After 1 and 4 weeks, scaffold integration and biocompatibility, axon sprouting, and myelination were evaluated. The chemically extracted acellular muscle scaffolds were found to be well integrated with the host tissue. Sprouting axons grew into the full length of the scaffold in a strikingly parallel and linear fashion. A few remyelinated axons were also detected in the scaffolds. The tracing results in another six rats showed that labeled fibers entered the chemically treated muscle grafts. Furthermore, there were no apparent quantitative differences in the ED-1 and glial fibrillary acidic protein positive cells between groups. Neuron counting showed more surviving neurons in the acellular muscle treated group than those of the injured only group. Vascularization of the grafts was also confirmed. These findings clearly demonstrated that chemically extracted acellular muscle grafts provided useful biomatrices to enhance axon sprouting in the injured spinal cord., (Copyright © 2011 Wiley Periodicals, Inc.)