RESUMEN
Objective:To investigate the effect of vagus nerve stimulation (VNS) on α7 nicotinic acetylcholine receptor (α7 nAChR) and inflammatory factor expressions and behavioristics in rats after traumatic brain injury (TBI).Methods:Seventy-two male Sprague-Dawley rats were randomly divided into sham-operated group, TBI group and VNS group ( n=24). The TBI models in the latter two groups were established by modified weight drop method; the dura mater in the sham-operated group was exposed without impingement. The VNS group received VNS treatment for 14 consecutive d (frequency: 30 Hz, pulse width: 100 μs, current: 0.8 mA, stimulation: 5 min, suspension: 5 min, repetition: 3 times). The neurological function was evaluated by Beam-Balance test and walking test 1, 3, 7, 14, 21, and 28 d after TBI; Morris Water Maze test was performed to observe the abilities of spatial learning and memory 24-28 d after TBI; the brain tissue sections were obtained for analyzing the volume of cerebral injury 28 d after TBI. Fourteen d after TBI, Nissel staining was used to observe the neuronal morphology and survival cell number of brain injured areas in each group, immunohistochemical staining was employed to detect the number of neuronalnuclear antigen (NeuN) positive neurons in the hippocampal dentate gyrus and CA3 area, and ELISA was used to detect the expressions of interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)-α and nuclear factor (NF)-κB. Western blotting was used to detect the α7 nAChR protein expression levels 3, 7, 14 d after TBI. Results:As compared with the TBI group, the VNS group showed statistically longer beam-balance latency and shorter beam-walking time 7, 14, 21, and 28 d after TBI, significantly shortened escape latency and prolonged exploration time in the target quadrant 27 and 28 d after TBI ( P<0.05). The volume of cerebral injury in the VNS group was significantly smaller than that in TBI group 28 d after TBI ( P<0.05). As compared with those in the TBI group, the number of Nissel positive neurons around the brain injury area was significantly larger, the number of NeuN positive cells in the hippocampal dentate gyrus and CA3 areas was significantly larger, and the expression levels of IL-1β, IL-6, TNF-α and NF-κB were significantly decreased in the VNS group 14 d after TBI ( P<0.05). The α7 nAChR protein expression in the injury area of VNS group was significantly higher than that of the TBI group 7 and 14 d after TBI ( P<0.05). Conclusion:VNS treatment can improve the neurobehavioral outcome of TBI rats, which may be linked with the increased α7 nAChR protein expression, and the decreased release of inflammation cytokines IL-1β, IL-6, TNF-α and NF-κB.
RESUMEN
BACKGROUND: In recent years, with the progress of shock therapy as well as the establishment and promoted application of arterial bypass grafting, thrombolytic therapy, percutaneous transluminal coronary angioplasty, extracorporeal circulation on cardiac surgery, cardiopulmonary resuscitation, limb replantation, and organ transplantation, blood reperfusion in multiple organs after ischemia has been achieved. However, the organs which undergo a period of ischemia appear to have the performance of damage aggravation.OBJECTIVE: To summarize the research progress of MG53 protein in protecting five organs from ischemia/reperfusion injury, thereby providing reference for further in-depth study.METHODS: A computer-based online search of PubMed, Duxiu Knowledge Search and CNKI databases was performed for relevant literatures puldished between 1986 and 2016. The key words were MG53, TRIM, Mitsugumin53, ischemic, reperfusion, preconditioning, postconditioning, RISK, membrane damage, Connexin43, KChIP2 in English and MG53, ischemia/reperfusion in Chinese. Finally 61 eligible articles were reviewed in accordance with the inclusion and exclusion criteria. RESULTS AND CONCLUSION: As a muscle-specific TRIM family protein, endogenous MG53 is involved in the repair of muscle cytomembrane damage, and the protective effects of ischemic preconditioning and postconditioning. Exogenous recombinant human MG 53 protein not only repairs membrane damage of various muscles and non-muscle cells, but also protects the myocardium, skeletal muscle, brain, lung and kidney from ischemia/reperfusion injury.
RESUMEN
Objective:To study the protective effect of platelet-rich plasma on never function in the rats with traumatic brain injury (TBI),and to clarify its mechanisms. Methods:Sixty SD rats were randomly divided into sham group (opened skull bone window only),TBI group and platelet-rich plasma treatment group (PRP group) (n=20).The rats in PRP group were injected with platelet-rich plasma through vessel on the 1st day,the 2nd day and the 6th day after operation while the rats in sham group and TBI group were treated with saline at the same time.The neurological function defects were assessed with modified neurological severity score (mNSS)on the 1st, 3rd and 7th after operation.Then 10 rats were taken from each group and executed,and the brain tissues were taken.The brain sections were prepared for the histological observation and the others of each group were tested with Morris water maze.Results:Compared with sham group,the mNSS scores of the rats in TBI and PRP group were increased (P <0.05);the mNSS score of the rats in PRP group was decreased compared with TBI group (P <0.05).The injured volume of rat brain tissue was reduced significantly in PRP treated group compared with TBI group (P <0.05).The Nissl staining results showed that the injury area in PRP group had a more neat rows and a larger number of new blood vessels compared with TBI group.The immunohistochemical staining results showed the injured area had a higher level expression of GFAP+ cells in TBI group compared with PRP group,but the amount of neuN+ cells was smaller than that in PRP group (P <0.05).The Morris water maze test results showed that there were a shorter escape latency time,more times acrossing platform and a larger swimming time during platform quadrant in PRP group compared with TBI group (P < 0.05).Conclusion:Platelet-rich plasma has a significant role in protecting the neurological function of TBI rats.
RESUMEN
Objective To explore the effects and mechanism of implantation of umbilical blood mesenchymal stem cells(MSCs)on rats with cerebral infarction. Methods Umbilical blood MSCs were cultured in vivo,flow cytometry was ap-plied to test cytometric immunophenotype, and model of rat cerebral infarction was made by suture method; 120 rats were randomly assigned to MSCs implantation group and control group; rats' neurological function was evaluated;western-blot was applied to test the expression of GFAP protein. Fluorescence microscope was applied to observe changes of hippocampal formation in rats as well as the distribution of MSCs in rats' brain. Results According to the test of neurological function, the score of neurological function in the experiment group was reduced, and the score in the control group was improved. The difference was statistically significant(P<0.05). Expression of GFAP in MSCs im-plantation group was increased with a peak in the 7th day,while no significant changes in the control group(P<0.05). According to the observation of immunofluorescence microscopy, the distribution of MSCs in rats' brain was good in MSCs implantation group, and the hippocampal formation showed clear layers in the experiment group. Hippocampal structures in the control group were chaotic, and synapses and organelles were dissolved and compromised. Conclu-sion MSCs are able to promote the repair of hippocampal structures after cerebral infarction in rats, strengthen neuro-plasticity and promote the recovery of neurological functions.
RESUMEN
Objective To study the effect of basic fibroblast growth factor(bFGF) on neuron-like differentiation of superparamagnetic iron oxide nanoparticles (SPIONs)-labeled amniotic membrane-derived mesenchymal stem cell.Methods Cells were cultured from enzymatic-digested amniotic membrane tissue.After that,the following steps were taken:(1) Mesenchymal stem cells derived from amniotic membrane were identified by using cell morphology,MTT method and flow cytometry.(2)SPIONs were used to label amniotic membrane-derived mesenchymal stem.(3)bFGF was imported to induce the neuron-like differentiation of SPIONs-labeled amniotic membrane-derived mesenchymal stem cell.Results (1) Primary cultures of P3,amniotic membrane-derived mesenchymal stem cell were fibroblast-like and expression of surface molecules CD29,CD44,CD90 and CD105 was detected,while expression of CD31,CD34,CD45 and CD106 was negative.(2) SPIONs of no more than 14.0 μg/ml are safe to label amniotic membrane-derived mesenchymal stem cells.Cell activity is more than 80％ and expression of surface molecules CD29,CD44,CD90 and CD105 is positive.(3)RT-PCR and immunocytochemistry analysis showed that 10.0 ng/ml bFGF induced neuron-like differentiation of amniotic membrane-derived mesenchymal stem cell (14 μg/ml SPIONs-labeled).Conclusions Enzymatic digestion and cell adherent culture method can be used to isolate mesenchymal stem cells from amniotic membrane.SPIONs of no more than 14.0 μg/ml are safe to label amniotic membrance-derived mesenchymal stem cells and have no effect on the cell activity.Neuron-like differentiation of amniotic membrane-derived mesenchymal stem cell can be induced with 10.0 ng/ml bFGF.
RESUMEN
Objective To study the effects of Genistein - magnetic - nanoparticles at different concentrations on the growth and ex-pression of focal adhesion kinase (FAK) in human hepatocellular carcinoma cell line HcpG2. Methods Activities of HepG2 cells treated by Genistein - magnetic - nanoparticles were examined by MTT assay. The expression of FAK mRNA and protein was respectively detected by immunohistochemistry staining and reversed transcriptase polymerase chain reaction (RT - PCR) . Results Genistein - magnetic -nanoparticles at a concentration of 10 -80mg/L inhibited the proliferation of HepG2 cells, with obvious concentration - dapendent and time - dependent effect relationships (P < 0.05). After treatment with various concentrations of Genistein - magnetic - nanoparticles for 48h, the relative level of FAKmRNA of Genistein - magnetic - nanoparticles and control groups was 1.242 ± 0.031,1.213 ± 0.443,0.834 ± 0.044,0.652 ± 0.039,0.446 ± 0.041, and 1.443 ± 0.053 (F = 21.97 ,P < 0.05), respectively. The expression of FAK protein in the cells was decreased, which showed an obvious a concentration - effect relationship. Conclusion Genistein - magnetic - nanoparticles can reduce the mRNA and protein expressions of FAK and inhibit the proliferation of HepG2 cells.
RESUMEN
Objective To study the effects of Genistein-magnetic-nanoparticles at different concentrations on the growth and expression of focal adhesion kinase(FAK) in human hepatocellular carcinoma cell line HepG2.Methods Activities of HepG2 cells treated by Genistein-magnetic-nanoparticles were examined by MTT assay.The expression of FAK mRNA and protein was respectively detected by immunohistochemistry staining and reversed transcriptase polymerase chain reaction(RT-PCR).Results Genistein-magnetic-nanoparticles at a concentration of 10-80mg/L inhibited the proliferation of HepG2 cells,with obvious concentration-dapendent and time-dependent effect relationships(P