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Objective:Reactive oxygen species (ROS) are significantly upregulated after spinal cord injury (SCI). MicroRNAs (miRNAs) are reported to be widely involved in regulating gene expression. This paper aims to explore the correlation between ROS-induced cell apoptosis and abnormal miRNA expression after SCI.Methods:To profile the expression of miRNAs after SCI, miRNA microarray was applied and the result was verified by reverse transcription quantitative PCR (RT-qPCR). ROS production following H2O2 stimulation was examined using dihydroethidium staining and flow cytometry. The levels of miR-200c after H2O2 treatment were determined using RT-qPCR. Cell viability and apoptosis were examined in murine BV-2 cells transfected with miR-200c mimics, inhibitor or negative control. Immunofluorescence and western blot were used to further explore the effects of miR-200c on Fas-associated phosphatase-1 (FAP-1) expression.Results:MiR-200c was showed to be significantly increased after SCI by miRNA microassay and RT-qPCR. ROS production enhanced miR-200c expression in a dose-dependent manner and induced significant apoptosis in BV-2 cells. The upregulation of miR-200c reduced cell viability and induced BV-2 cell apoptosis. MiR-200c negatively regulated the expression of FAP-1, thereby inducing FAS signaling-induced apoptosis. RT-qPCR analysis showed that the FAP-1-targeting small interfering RNA (siRNA) did not affect the level of miR-200c in murine BV-2 cells. In addition, suppression of FAP-1 by siRNA promoted apoptosis, even in cells that were co-transfected with the miR-200c inhibitor.Conclusions:The current data suggested that miR-200c contributes to apoptosis in murine BV-2 cells by regulating the expression of FAP-1. This proposes a therapeutic target for enhancing neural cell functional recovery after SCI. [ABSTRACT FROM AUTHOR]

Study design:Experimental study.Objectives:To investigate whether Bosentan, an endothelin-A/-B dual receptor antagonist, could protect neurons after spinal cord ischemia reperfusion (SCIR) injury in rats and its underlying signaling pathway.Setting:Department of Neurosurgery, the Second Affiliated Hospital, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi Province, China.Methods:Sprague-Dawley rats were randomly divided into two groups, saline group (IRS, n=48) and Bosentan group (IRB, 5 mg kg−1, n=48). After ischemia for 1 h with occlusion of the infrarenal aorta, spinal cord were reperfused for 6h, 12h, 24h, 3d, 5d, and 7d separately. Enzyme-linked immunosorbent assay was used to detect vascular endothelial growth factor (VEGF) in serum. Immunohistochemistry was performed to detect protein expression of VEGF, VEGF receptor 1 (FLT-1) and VEGF receptor 2 (FLK-1). Gene expressions of VEGF and its receptors were evaluated using the quantitative reverse transcription polymerase chain reaction.Results:Compared with the IRS group, gene and protein expressions of VEGF, FLT-1 and FLK-1 were significantly increased (P<0.05), so was the concentration of VEGF in plasma (P<0.05). FLK-1 was expressed on spinal cord neurons. [ABSTRACT FROM AUTHOR]

Objectives:The aim of this study was to determine the therapeutic effects of a collagen scaffold-collagen binding brain-derived neurotrophic factor (CBD-BDNF) complex (CSCB) on behavioral, electrophysiological and histological improvements in canine complete spinal cord transection model.Methods:A total of 24 adult female beagle dogs received a complete spinal cord transection at the T12 level in three groups, including SHAM group (n=8), CTL group (complete spinal cord transection without any treatment, n=8) and CSCB group (complete spinal cord transection with CSCB, n=8).Results:CSCB therapeutic group showed markedly functional recovery by Olby score and spinal somatosensory evoked responses (SSERs) assay at 12 weeks after complete spinal cord transection. Furthermore, numerous peripheral myelinated axons aligned parallel to the long axis of the spinal cord were detected in CSCB group dogs. In stark contrast, the injured site was dominated by fibrous and only scattered axons were detected in the edge of spinal cord in CTL group dogs.Conclusion:The CSCB has an evident therapeutic effect by facilitating peripheral nerve infiltrating following the severe spinal cord injury in canine animals. [ABSTRACT FROM AUTHOR]

Objectives:To evaluate the effects of different doses of ascorbic acid (AA) on the functional performance of rats subjected to standardized spinal cord injury (SCI).Methods:Thirty female Sprague-Dawley rats were divided into three groups (10 animals in each group): control group: rats were subjected to SCI injury and received intraperitoneal saline administration; normal-dose AA group: rats were subjected to SCI injury and received daily intraperitoneal administration of AA at 100 mg kg−1 bodyweight; high-dose AA group: rats were subjected to SCI injury and received daily intraperitoneal administration of AA at 200 mg kg−1 bodyweight. The Basso, Beattie, Bresnahan Locomotor Rating Score (BBB score) and footprint analysis were performed to evaluate the functional performance of the rats in each group, and hematoxylin and eosin staining was performed to evaluate necrosis at the injury site.Results:At days 14 and 28 after SCI, rats in the high-dose AA group, but not the normal-dose AA group, exhibited significantly better BBB score compared with the control group (P<0.05). Compared with the control and normal-dose AA group, the high-dose AA group also showed increased stride length, decreased stride width and reduced toe dragging (P<0.05). Histological analysis revealed that both the normal- and high-dose AA groups had reduced necrosis in the injury site compared with the control group (P<0.05).Conclusion:High-dose AA administration during the acute phase post SCI significantly reduced secondary injury-induced tissue necrosis and improved functional performance in rats. [ABSTRACT FROM AUTHOR]