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目的观察减压性中枢神经系统损伤及高压氧(HBO)处理后小胶质细胞活性的变化,探讨小胶质细胞在减压性中枢神经损伤中的作用及其可能的机制与HBO效用的机制。方法动物分为正常对照组、安全减压对照组、致伤组、HBO治疗组。以不安全快速减压大鼠中枢神经损伤模型为实验对象,致伤后6h给予HBO处理。观察活化小胶质细胞、TNF-α/TACE免疫阳性细胞、神经细胞凋亡,组织内TNF-α含量和脑脊液(CSF)内TNF-α的生物活性。结果损伤后6h就可见脑和脊髓组织内IB4阳性活化小胶质细胞,数量的高峰出现在24h,活化的小胶质细胞出现形态改变。神经元凋亡在损伤后48h达到高峰。小胶质细胞出现的区域与神经细胞凋亡出现的区域相同。损伤后6h就可在CNS组织中检测到TNF-α,48h达到高峰,与IB4阳性细胞及神经细胞凋亡指数呈正相关(P<0.05)。CSF中TNF-α的生物活性也出现相同的变化趋势。TNF-α和TACE免疫阳性细胞形态和分布与IB4阳性细胞类似。HBO治疗可显著减少中枢神经组织中活化小胶质细胞的数量,降低组织和CSF中TNF-α的含量,减少神经细胞凋亡。结论减压性损伤中枢神经组织内小胶质细胞迅速激活,后者增加毒性物质的表达和分泌,介导继发损伤。HBO能够抑制小胶质细胞反应,降低其活性,减少毒性物质的分泌,起到神经元保护作用。
Objective To observe the changes of microglial activity after stress-induced central nervous system injury and hyperbaric oxygen (HBO) treatment and to explore the role of microglia in the decompression central nervous system injury and its possible mechanism and mechanism of HBO utility . Methods Animals were divided into normal control group, safe decompression control group, injury group and HBO treatment group. The model of central nervous system injury in rats with unsafe and rapid decompression was used as experimental object, and HBO treatment was given 6h after injury. The activated microglial cells, TNF-α / TACE immunopositive cells, neuronal apoptosis, TNF-α content in the tissues and biological activity of TNF-α in cerebrospinal fluid (CSF) were observed. Results 6 hours after injury, IB4-positive activated microglial cells in brain and spinal cord tissue were observed. The number peak appeared at 24h and the activated microglial cells showed morphological changes. Neuronal apoptosis peaked 48h after injury. The area where microglia appear is the same as the area where neuronal apoptosis occurs. TNF-α could be detected in CNS tissue 6h after injury, and peaked at 48h, which was positively correlated with IB4-positive cells and neuronal apoptosis index (P <0.05). The biological activities of TNF-α in CSF also show the same trend. The morphology and distribution of TNF-α and TACE immunopositive cells were similar to those of IB4-positive cells. HBO treatment can significantly reduce the number of activated microglial cells in the central nervous system, reduce the level of TNF-α in the tissues and CSF, and reduce the apoptosis of nerve cells. Conclusions The microglial cells in the central nervous system of rats with decompression injury rapidly activate, while the latter increase the expression and secretion of toxic substances and mediate the secondary injury. HBO can inhibit microglial response, reduce its activity, reduce the secretion of toxic substances, play a neuroprotective role.