BACKGROUND:Neurotrophic factors have been conformed to have the effects of promoting the survival, differentiation and axonal regeneration of the injured neurons, so that the structural integrity of the injured spinal cord can be reserved as much as possible.OBJECTIVE: To observe the effects of nerve growth factor (NGF) on the neural regeneration and motor function following spinal cord injury in rats.DESIGN: A randomized controlled observation.SETTING: Department of Neurology, Union Hospital affiliated to Tongji Medical College, Huazhong University of Science and Technology.MATERIALS: Thirty healthy adult male Wistar rats of common degree, were provided by the Experimental Animal Center, Tongji Medical College of Huazhong University of Science and Technology.METHODS:The experiment was carried out in the Department of Neurology, Union Hospital of Tongji Medical College,Huazhong University of Science and Technology. The 30 rats were randomly divided into NGF-treated group (n=15) and control group (n=15). ① T8 spinal injury was induced by the improved Allen method. ③ The improved Rivlin method (namely, slope test) was used to assess the motor function following spinal cord injury in rats before model establishment and at 3 days, 1, 2 and 3 weeks after treatment respectively. ④ At 2 days and 3 weeks postoperatively, 7 rats in the NGF-treated group and 8 rats in the control group were selated and the cross-sectional tissue(0.5 cm) of the injured spinal cord was removed, fixed in neutral formalin, dehydrated, and embedded with paraffin, and then cut into 5 μm sections.MAIN OUTCOME MEASURES:① The results of the slope test before model establishment and at 3 days,1, 2 and 3weeks after treatment respectively; ② Axonal count in white matter at 2 days and 3 weeks after model establishment.RESULTS:① The scores of slope test after spinal cord injury at 1, 2 and 3 weeks postoperatively in the NGF-treated group were obviously higher than those in the control group [(45.2±3.2), (51.2±3.8), (53.4±4.6)°; (45.2±3.2), (51.2±3.8),(53.4±4.6)°, P ＜ 0.05].② At 3 weeks after treatment, a few dispersal and heterogeneous NGF200 spots were observed in the white matter of rats in the control group, but there were plentiful and symmetrical NGF200 spots in the NGF-treated group. The axonal count in white matter at 3 weeks following spinal cord injury in the NGF-treated group was obviously higher than that in the control group (363.6±34.2, 187.5±32.1, P＜ 0.05).CONCLUSION:NGF can promote the neural regeneration following spinal cord injury to a certain extent, and help to im prove the functional recovery.

61mg/L. Conclusion The destruction of blood-brain barrier in TM and PM was obviously stronger than that in VM. The contents of CSF-Ig and -Alb are helpful to diagnose and differntially diagnose meningitis.

Objective To investigate the effect of Exelon on cognitive function of chronic cerebral hypoperfusion rats and its cholinergic mechanism.Methods 112 rats were randomly separated into four groups (normal, hypoperfusion, normal saline and Exelon). Bilateral common carotid arteries were ligated for models of cerebral hypoperfusion in the rats except normal group. 4 weeks later, Exelon and normal saline were used to treat the rats in Exelon group and normal saline group respectively for 6 weeks. Then the values of AchE lever and Ach fiber density together with the results of experiments in water maze and the values of event-related potential (ERP) were recorded and compared with each group.Results Comparing with the normal group, the water maze completion time of the hypoperfusion group was significantly delayed, error frequency significantly increased, the latency of ERP much extended, the AchE level and Ach fiber density evidently decreased(all P

AIM To investigate antiplatelet agents induced neuroprotection, which is blood perfusion independent, and its gender difference. METHODS Population spike amplitude (PSA) was measured during hypoxia and posthypoxic recovery in blood fsee hippocampal slices from untreated control mice and from in vivo pretreated mice with a single intraperitoneal injection of acetylsalicylic acid (ASA), ticlopidine or clopidogrel. Extracellular recordings and NADH fluorescence spectroscopy were used to determine PSA and NADH fluorescence upon hypoxia in CA1 region in hippocampal slices from ASA treated male and female mice. RESULTS Posthypoxic recovery of PSA was 25 9%?11 6% in control slices. In slices pretreated with ASA, ticlopidine and clopidogrel PSA recovered to 74 7%?35 7% ( P

Objective To investigate the effect of Aricept on the level of cholinesterase and the density of cholinergic fibres in cortex of frontal lobe and hippocampus zone in rats undergoing chronic cerebral hypoperfusion rats. Methods One hundred and twelve male SD rats were divided into a normal group, a model group, a saline treatment group (saline, 3mg/kg/day for six weeks) and an Aricept treatment group (Aricept, 3mg/kg/day for six weeks). After six weeks of treatment, all rats were tested with water maze, and then the level of cholinesterase and the density of cholinergic fibres were detected. Results The performance of the rats of the model group with water maze were worse than that of the normal group (P

Objective To establish a novel model of senile dementia in rats. Methods Fifty-two Wistar male rats were divided into 5 groups, group A was treated with a permanent bilateral occlusion of both carotid arteries (2-VO) first and then intraperitoneal injection of D-galactose (60 mg?kg -1 ?d -1 ,ip,42 d), group B with intraperitoneal injection of D-galactose (60 mg?kg -1 ?d -1 ,ip,42 d) first and then permanent bilateral occlusion of both carotid arteries, group C with 2-VO, group D with intraperitoneal injection of D-galactose, and group E (normal control) without the above treatment. All the rats were tested by using Morris water maze for their performance in learning and memory. Results Wistar rats treated with both 2-VO and D-galactose presented a significant diffe-rence from those simply treated by 2-VO and the normal rats. Conclusion The rat model of senile dementia induced by 2-VO and D-galactose simulated some characteristics of human senile dementia, and might be used in basic experiment study of senile dementia, such as vascular dementia, Alzheimer′s disease and mixed dementia.

Objective To evaluate the effects of TMS on the brain plasticity and functional outcome after cerebral infarction in rats. Methods Twenty-four male Sprague-Dawley rats were divided randomly into a model group and a TMS group. The rat models of focal cerebral infarction were established with unilateral middle cerebral artery (MCA) suture occlusion method. The rats of TMS group were given additional 4 weeks of TMS treatment commenced at!1 day after infarction (2 times per day, 30 pulses per time), while those in the control group were reared in their original living state. Synaptic substructure in the sensori-motor cortex area was assessed morphologically and quantitatively. Results When compared with the model group, the rats in the experimental group had a significant improvement in terms of their neural functions (P

Objective To study the effects of transcranial magnetic stimulation (TMS) on the expression of c-Fos and brain-derived neurotrophic factor (BDNF) of the cerebral cortex in rats with cerebral infarction. Methods Cerebral infarction models were established by using of left middle cerebral artery occlusion (MCAO) and randomly divided into a model group (n=40) and a TMS group (n=40), in additional, TMS treatment (2 times per day, 30 pulses per time) with frequency of 0.5 Hz and magnetic field intensity of 1.33 Tesla was carried out in TMS group after infarction. The expression of c-Fos and BDNF was measured at 1 d, 7 d, 14 d, 21 d and 28 d after infarction, respectively. Results The positive expression c-Fos and BDNF was detected in the cortex around the infarction areas, while the expression of c-Fos and BDNF was increased significantly in TMS group in comparison to those in model group at 7 d, 14 d, 21 d, 28 d (P

Objective To investigate the effect and its mechanism of cyclin dependent protein kinase inhibitor Olomoucine treatment on experimental herpes simplex encephalitis(HSE). Methods 45 mice were randomly assigned to HSV-1 sham-infected group (n=15), HSV-1 infected control group (n=15) and Olomoucine treated group (n=15). Flow cytometry was used to detect the expression of brain cells surface antigen CD11b. The reverse transcription polymerase chain reaction (RT-PCR) to detect the expression of tumor necrosis factor-? (TNF-?) and Interleukin-6 (IL-6). TUNEL method was adopted to detect neural cells apoptosis. Pathologic slices of brain tissues were used to identify tissue morphology differences. The survival rates were compared between the treatment groups Acyclovir (n=20) and Olomoucine (n=20) by the method of Kaplan-Meier 2 weeks after HSV-1 infection. Results After HSV-1 infection, the expression of brain tissue CD11b, TNF-?, IL-6 were significantly increased compared with sham-infected group (allP

BACKGROUND: Transformation growth factor β1 (TGF-β1) can promote bone marrow mesenchymal stem cells (BMSCs) migration and proliferation, but the underlying mechanisms remain unclear.OBJECTIVE: To observe the invasiveness of TGF-β1 on BMSCs cultured in vitro, and to investigate regulatory effect on Snail and matrix metalloproteinase 2 (MMP-2) expression.METHODS: Rat BMSCs were isolated and cultured with density gradient centrifugalization and adherence method. The influence of different concentrations of TGF-β1 on the BMSC migration was detected using the modified Transwell chambers. Small interfering RNA for Snail gene was synthesized and transfected into BMSCs by liposomel before TGF-β1 was treated, and the expression of Snail and MMP-2 before and after transfection were measured by western blot assay.RESULTS AND CONCLUSION: The exogenous TGF-β1 can induce a dose-dependent increase in cell migration, which peaked at 2 μg/L. The expression levels of Snail mRNA and MMP-2 mRNA were significantly increased after 2 μg/L TGF-β1 treatment. Snail gene can effectively inhibit the expression of MMP-2 promoted by TGF-β1. Experimental findings indicate that TGF-β1 could increase the MMP-2 expression and then promote the BMSCs migration through the upregulation of the Snail expression.