The Role Of S100-? Protein In The Pathological Mechanism Of Spinal Cord Injury

Background:Spinal cord injury(SCI)refers to a central nerve caused by trauma,inflammation,tumor and other causes,with the same clinical outcomes,a high disability rate,high mortality rate,and no effective method to cure Systemic diseases can cause transverse spinal cord injury,resulting in impairment of motor,sensory,sphincter and autonomic dysfunction below the level.The occurrence and development of spinal cord injury is accompanied by a strong and sustained inflammatory response.The infiltration of inflammatory cells and the release of inflammatory factors can cause the scope of injury to expand rapidly and exacerbate the necrosis of surrounding tissues.Among them,microglia(MG),which is widely present in the central nervous system,can be activated by tissue factor to transform into the M1 phenotype after spinal cord injury,and activate the intracellular inflammatory level by phagocytosis of necrotic cell fragments Synergistic reaction,release a large number of pro-inflammatory factors,including IL-6,IL-1?,TNF-a,MHC-II,i NOS and ROS,etc.,aggravate the inflammatory response in the tissue microenvironment,which in turn damages the surrounding normal spinal cord tissue,causing inflammation Range spread.The study found that in neurological diseases and injuries caused by various reasons,the s100-? protein secreted by astrocytes and oligodendrocytes has a certain degree of increased secretion,and the extracellular space is more The high concentration of s100-? protein may induce astrocytes to produce i NOS,thereby promoting the expansion of DNA damage or apoptosis.There is an unclear correlation between s100-? protein and nervous system injury.Clarifying the interaction between s100-? protein and related inflammatory cells and inflammatory factors may advance the research on the pathogenesis of spinal cord injury.Function,and thereby bring about the effect of optimizing the treatment plan of spinal cord injury.Therefore,it is necessary to further demonstrate the role of microglia and s100-? protein in the design of spinal cord injury pathological mechanisms.Objective:This study attempts to analyze the pathological processes of tissue inflammation activation,gene and protein expression,and release of inflammatory factors to clarify the response and change trend of s100-? protein and microglia after spinal cord injury,in order to further explore the two The mechanism of action between them provides a theoretical basis and provides new arguments and ideas for studying the pathological changes of spinal cord injury.Method:The design of this study is divided into two parts: animal experiments and cell experiments.Animal experiments use C57 B / 6J mice to build an animal model of spinal cord injury.Cell experiments use LPS to induce BV-2 cells to build a microglia activation model.Experiments use immunofluorescence markers,Western blot and q RT-PCR experimental techniques were used as analysis methods.By analyzing the expression of S100-? protein,activation of microglia,and the release of inflammatory factors after spinal cord injury,the role of S100-? protein in the pathological mechanism of spinal cord injury was described.Result:Animal experiments successfully constructed a mouse spinal cord injury model.In the early stage of spinal cord injury,the spatial distribution of S100-? protein was highly consistent with activated microglia;further quantitative analysis found that the activation of microglia M1 type increased,S100-? protein and Upstream genes are highly expressed,and tissue proinflammatory factors are released.Over time,S100-? protein,microglia,and pro-inflammatory factors all fell back to normal levels 14 days after injury.In cell experiments,BV-2 cells can be activated to the M1 phenotype by LPS treatment,successfully constructing a microglia activation model.In activated microglia,S100-? protein,M1 phenotypic markers,and tissue pro-inflammatory factors all showed an increasing trend,and high expression at multiples of normal levels could be achieved within 24 hours.Conclusion:Based on the experimental results of this study,it was found that S100-? protein was significantly over-expressed in the early stage of spinal cord injury,accompanied by increased activation of microglia M1 phenotype and increased expression of tissue proinflammatory factors.S100-? protein may be secreted by microglial cells that rapidly activate to M1 type after spinal cord injury,and further interact to strengthen the expression of tissue proinflammatory factors and aggravate the inflammatory response of injured tissues.The mechanism of action between the two needs to be further designed Experimental analysis and demonstration.