Objective To study the role of activated microglia transplantation in recovery of hindlimb locomotor function in rats with spinal cord injury(SCI). Methods A total of 40 female adult Wistar rats were selected and divided into four groups randomly(10 rats in each group).The former two groups were locomotor function observation groups,in which rat model with spinal cord was established by striking with improved self-made Allen's strike equipment to fabricate moderate spinal cord injury and divided into transplantation group and control group.The latter two were histological observation groups,the spinal cord injury model was fabricated by the same above-mentioned method and divided into transplantation and control groups.Before fabricating the spinal cord injury model,the microglia of the newborn rats were cultured,separated,purified and identified and the purity of the microglia determined.The injury position was exposed again seven days after transplantation and the cell suspension of microglia was injected around the injury position with microsyringe,which was free in the control group.The hindlimb locomotor function of rats was detected and scored at 1 day,1,2,3 and 4 weeks in the locomotor function observation groups after transplantation respectively.At the same time,two rats were extracted randomly from the control group and the transplantation group in histological observation groups to cut specimen and slice for Naoumenko-Feign paraffin section and dying.Then,the microglia were observed and counted by microscope and analyzed statistically. Results At 1,2,3 and 4 weeks after operation,the BBB score of the control group and the transplantation group was increased gradually with the time.But compared with the control group,transplantation group had higher scores of hindlimb locomotor function at 2,3 and 4 weeks after operation,with statistical difference(P＜0.05).Naoumenko-Feigin paraffin section and dying and microglia counting showed that positive microglia number in the transplantation group was increased more obviously than the control group,with statistical difference(P＜0.05).Conclusion Activated microglia transplantation can promote the recovery of the hindlimb locomotor function in SCI rats.

Objective To detect the expression pattern of microRNA in A549 cells treated by lipopolysaccharide, study the expression of miRNA-1247-3P in A549 cells under LPS treatment and explore the possible mechanism of miRNA-1247-3P in A549 cells under LPS treatment. Methods A549 cells were divided into experimental and control groups. Immunocytochemical method and RT-PCR were used to detect the changes of SP-A and SP-C. The expression of miRNAs were detected using miRNAs array in different groups. The key miR-1247-3P was collected to detect the changes of miR-1247-3P in all groups using quantitative real-time polymerase chain reaction. Results Compared with control group, the expressions of SP-A and SP-C were significantly decreased in the experimental groups (P < 0.05). MiRNA array showed that 31 miRNAs were up-regulated and 3 miRNAs were down-regulated. Compared with control group, the expression of miR-1247-3P was significantly increased in the experimental groups (P < 0.05). Conclusion The increased expression of miR-1247-3P may play an important role in the pathogenesis of ARDS.

ObjectivesTo investigate the expression of glucose regulated protein 78 (GRP78), CCAAT/enhancer binding protein homologous protein (CHOP) and cysteine asparate protease-12 (caspase-12) and neuronal apoptosis in the brain of zebraifsh larvae after hypoxia reperfusion, and the neuroprotective effect of taurine.Methods Five day old post-fertilization zebraifsh larvae were randomly assigned into 3 groups, control group, hypoxia reperfusion group (model group) and taurine group, and the taurine group was further divided into 3 subgroups according to different concentrations (1 mmol/L, 5 mmol/L, 10 mmol/L) with 100 zebraifsh larvae each. The behavior, recovery time and median survival time of those zebraifsh larvae after hypoxia with 1h reperfusion were observed and recorded. The pathological changes and apoptosis of neurons were detected by Nissl staining and terminal deoxynucleotidyltransferase-mediated dUTP nick end-labeling. The expression of GRP78, CHOP and caspase-12 in the brain of zebrafish larvae were detected by Western blot.Results Compared with the model group, the recovery time was shortened, the median survival time was extended, the Nissl stained neurons was increased and the apoptotic neurons were decreased in the taurine groups. GRP78, CHOP and caspase-12 were expressed in model group and taurine group. The expression of GRP78, CHOP and caspase-12 was much lower in taurine group than in model group.Conclusions Hypoxia reperfusion may induce endoplasmic reticulum stress and taurine may be neuroprotective against hypoxia reperfusion by down-regulating GRP78, CHOP and caspase-12.

Many factors,especially perinatal asphyxia,can lead to varying degrees of hypoxia brain injury in fetus or newborns within perinatal period.So far,the mechanisms of neonatal cerebral damage caused by hypoxia during the perinatal period have not been clearly demonstrated,and there have no effective drugs or therapeutic methods to improve hypoxia-induced cerebral damage.This review focuses on the recent progress of zebrafish as a model organism of using in research of hypoxia brain injury,including the anatomic and behavior basis,model making,research strategies and the advantages of neurotrophic drug screening.The application of zebrish in the research of neonatal hypoxic brain injury is promising,and may provide a new tool as research in finding out the therapy strategies of hypoxic-ischemic encephalopathy.

Brain injury is one of the most serious diseases in neonatal period,which can cause cerebral palsy,motor development delay,cognitive dysfunction and learning difficulties and other sequelae,and severely affects the health development and quality of life of the newborn.Neonatal brain injury (NBI) is a wide range of diseases caused by a variety of causes,its clinical manifestations lack specificity,clinically,it is difficult to judge the severity,duration and the time of prenatal injury,and it has been paid much attention to by scientific researchers and clinicians.At present,imaging method is a major means of NBI diagnosis,but imaging examination is usually a lag and limitations.Levels of humoral biomarkers change early after brain injury,and early brain injury can be predicted by detecting their changes.In recent years,a variety of sensitive brain damage biomarkers have been detected in various body fluids of newborns,mainly including neuron-specific enolase (NSE),ubiquitin carboxyl hydrolase L1 (UCH L1),S100B protein,tau protein,myelin basic protein (MBP),glial fibrillary acidic protein (GFAP) and activin A and so on.the application and research progress of these commonly used biomarkers in NBI are reviewed in this paper.

BACKGROUND:Foreign scholars have researched hypoxia reperfusion in zebrafish embryos, but there is no research on c-fos gene expression and the mechanism during zebrafish cerebral hypoxia reperfusion.
OBJECTIVE:To observe the zebrafish embryonic brain cel apoptosis and expression of c-fos gene in brain tissues after hypoxia reperfusion.
METHODS:Zebrafish embryos were selected at 48 hours post fertilization. Neonatal hypoxia reperfusion injury was simulated by gradual y leading nitrogen (99.999%) into the device. After hypoxia treatment for 6, 12 and 24 hours, the embryos received reperfusion for 6 hours under normal oxygen concentration. The embryos in the control group received normoventilation (the dissolved oxygen concentration was about 7.0 mg/L). Acridine orange staining was performed to observe the effect of different hypoxia durations on the apoptosis of neurons in zebrafish, and then the c-fos gene expression was quantitative analyzed with real-time quantitative nucleic acid amplification detection system. And the expression level of c-fos gene was compared before and after hypoxia reperfusion.
RESULTS AND CONCLUSION:A smal amount of apoptotic brain cel s could be detected in the control group, and the c-fos gene expression level was decreased;in the experimental group, the number of apoptotic cel s was increased after hypoxia for 6, 12 and 24 hours, and the gene expression after hypoxia for 6 hours was increased distinctly. The results indicate that hypoxia can increase the c-fos gene expression in brain cel s of zebrafish embryos, which may be one of the mechanisms of brain cel apoptosis increasing after hypoxia.

Objective To discuss the mechanism of miR-24-3P in the process of acute respiratory distress syndrome (ARDS).Methods miR-24-3P mimics,miR-24-3P inhibitor and their negative controls were transfected in RAW264.7 cells respectively:The relative expression of miR-24-3P in each cell was detected.The relative expression of TNF-α,IL-6,SP1 and NF-κB were detected in each cell,and the regulation of miR-24-3P on the target gene SP1 was detected by dual luciferase reporter gene.Results The expression level of TNF-α mRNA and IL-6 mRNA in each group was statistically significant (P＜0.05).The relative expression level of SP1 mRNA and NF-κB mRNA in each group was not statistically significant (P＞0.05).The expression of SP1 in each group was statistically significant (P＜0.05).The gene analysis of dual luciferase reporter showed that the fluorescence activity was significantly inhibited after cotransfection of miR-24-3P and SP1 in HEK293 cells(P＜0.05).Conclusion miR-24-3P can play an important role in the process of ARDS by influencing the translation of SP1 gene and affecting the release of inflammatory mediators.