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Objective To observe the effects of melatonin on synaptic plasticity impaired by spinal cord injury in rats. Methods A total of 54 female Sprague-Dawley rats were divided into sham group (n=18), control group (n=18) and melatonin group (n=18). Spinal cord inju-ry model was established with modified Allen's method at T10 (10 g from 25 mm height). The number of neurons and the expression of the Nissl body were detected with immunofluorescence and Nissl staining. The expression of neurofilament-200 (NF-200), brain-derived neuro-trophic factors (BDNF), Synapsin I and growth-associated protein-43 (GAP-43) was detected with Western blotting. Results Seven days af-ter injury, the number of motoneurons, the expression of Nissl body in motoneurons, and the expression of BDNF, Synapsin I and GAP-43 decreased in the control group compared with those in the sham group, and they increased in the melatonin group compared with those in the control group. Conclusion Melatonin can repair the impaired synaptic plasticity, which might promote the functional recovery after spi-nal cord injury.
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@#Objective To investigate the influence of matrix metalloproteinases-9 (MMP-9) on permeability of blood-spinal cord barrier (BSCB) after spinal cord injury (SCI). Methods 68 male C57BL/6 mice were randomly divided into sham group, 2 days group (S2), 7 days group (S7) and 14 days group (S14) after SCI with 17 mice in each group. All the groups received a moderate impacted spinal cord injury except the sham group. Evan's Blue (EB) was administered intraperitoneally to detect the permeability of BSCB. Occludin was analyzed by immunofluorescence, the expressions of occludin and MMP-9 were detected by Western blotting. Results After SCI, BMS score significantly reduced, compared with S2 group, S14 group showed a significant increase (P<0.01). The permeability of BSCB was seriously damaged after SCI. Compared with S2 group, S14 group showed a notable down-regulation in the permeability of injured micro-vessels (P<0.05). The expression of occludin was down-regulated and the expression of MMP-9 was up-regulated 7 days after SCI (P<0.05). Compared with S2 group, S14 group showed a significant up-regulation of occludin and a remarkable down-regulation of MMP-9 (P<0.05). Conclusion After SCI, MMP-9 might mediate the expression of occludin to influence the BSCB permeability.
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Objective To investigate the influence of matrix metalloproteinases-9 (MMP-9) on permeability of blood-spinal cord barrier (BSCB) after spinal cord injury (SCI). Methods 68 male C57BL/6 mice were randomly divided into sham group, 2 days group (S2), 7 days group (S7) and 14 days group (S14) after SCI with 17 mice in each group. All the groups received a moderate impacted spinal cord injury ex-cept the sham group. Evan's Blue (EB) was administered intraperitoneally to detect the permeability of BSCB. Occludin was analyzed by im-munofluorescence, the expressions of occludin and MMP-9 were detected by Western blotting. Results After SCI, BMS score significantly reduced, compared with S2 group, S14 group showed a significant increase (P<0.01). The permeability of BSCB was seriously damaged af-ter SCI. Compared with S2 group, S14 group showed a notable down-regulation in the permeability of injured micro-vessels (P<0.05). The expression of occludin was down-regulated and the expression of MMP-9 was up-regulated 7 days after SCI (P<0.05). Compared with S2 group, S14 group showed a significant up-regulation of occludin and a remarkable down-regulation of MMP-9 (P<0.05). Conclusion After SCI, MMP-9 might mediate the expression of occludin to influence the BSCB permeability.
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Objective To explore the change of proportion of peripheral blood dendritic cells (DCs) in patients with stroke. Methods 56 patients (30 cases of cerebral infarction and 26 cases of cerebral hemorrhage) in Beijing Bo'ai hospital from June to September, 2014 and 14 healthy controls were investigated. The severity of stroke was assessed with the National Institutes of Health Stroke Scale (NIHSS). Flow cy-tometry analysis was employed to detect the proportion of DCs subtypes in the peripheral blood. Results No obvious difference was found in DCs between the stroke patients and the controls. Compared to the control group, the percentages of peripheral blood myeloid dendritic cells (mDCs) decreased in the cerebral hemorrhage and the cerebral infarction subgroups (P7 subgroup. The percentages of pDCs in the cerebral hemorrhage and the cerebral infarction patients were significantly lower in the NIHSS>7 subgroup than in the NIHSS≤7 subgroup (P7 subgroups in the percentages of mDCs in the cerebral hemorrhage and cerebral infarction patients. Conclusion The proportion of DCs subtypes in the peripheral blood in stroke patients changed significantly, indicating inflamma-tion responds play a role in stroke.
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<p><b>BACKGROUND</b>Pericytes, located on microvessels, help to maintain vascular stability and blood-brain barrier integrity. The influence of pericytes on microvessels after spinal cord injury (SCI) is less clear. Therefore, the aim of this study was to investigate whether pericytes took a protective effect on microvessels in melatonin-treated SCI.</p><p><b>METHODS</b>C57BL/6 mice were randomly divided into three groups: sham group, SCI group, and melatonin group (n = 27 per group). Functional recovery was evaluated using the Basso Mouse Scale. Motor neurons were observed using hematoxylin and eosin staining. Pericyte coverage was analyzed using immunofluorescence. Permeability of blood-spinal cord barrier (BSCB) was assessed by administration of Evan's Blue. Protein levels of occludin, aquaporin-4 (AQP4), angiopoietin-1 (Ang1), intercellular cell adhesion molecule-1 (ICAM-1), Bcl-2, and Bax were determined using Western blotting. Mimicking the pathological conditions of SCI, melatonin-treated primary pericytes were subjected to oxygen-glucose deprivation/reperfusion (OGD/R). Secretion of Ang1 was analyzed using an enzyme-linked immunosorbent assay, and the expression of ICAM-1 was detected by immunofluorescence.</p><p><b>RESULTS</b>Melatonin treatment improved locomotor functional outcome and rescued motor neurons. Pericyte coverage was significantly reduced after SCI; melatonin treatment alleviated the loss of pericyte coverage and rescued perfused microvessels 7 days after injury. The permeability of BSCB and loss of occludin were attenuated, and edema formation and upregulation of AQP4 were inhibited, after melatonin treatment. The expression of Ang1 and Bcl-2 was improved, while the expression of ICAM-1 and Bax was inhibited, in melatonin-treated SCI mice. Furthermore, the secretion of Ang1 was increased and the expression of ICAM-1 was inhibited in melatonin-treated pericytes after OGD/R.</p><p><b>CONCLUSIONS</b>Melatonin ameliorated the loss of blood vessels and disruption of BSCB to exert a protective effect on SCI, which might be mediated by increased pericyte coverage. The upregulation of Ang1 in pericytes could inhibit inflammation and apoptosis to protect the microvessels.</p>