ACTA NEUROPHARMACOLOGICA

Effects of Low-dose Methotrexate on Spinal Cord Contusion-Induced Neural Cell Apoptisis in Rats

ZHANG Si, WANG Shuo-yu, GU Bing, LI Hua-nan, ZHANG Guo-fu, ZHANG Shui-yin

2013, 3 (6): 1-8.

Abstract ( 2720 )

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Objective：This study examined the effect of low-dose methotrexate on spinal cord contusion–induced neural cell apoptosis in rats and its potential protective mechanism. Methods: Rat spinal cord contusion model was established by Pinpoint Precision Cortical Impactor™ apparatus and then methotrexate (0.3 mg • kg^-1• BW) was subcutaneously administrated daily for 2 weeks starting from 30 min post-injury. Immunohistochemical staining and TUNEL method were used to examine the expression of neuronal nuclear antigen (NeuN) and neural cell apoptosis at damaged area, respectively. Results: One day after the traumatic injury, gray and white matter structures were unaltered and neuronal necrosis was only noticeable at the epicenter. TUNEL-positive cells were primarily located in the posterior horn of gray matter. 3～7 days after injury, the TUNEL-positive cells were increased and the location of these cells spreaded to the ventral and diffused periphery sections of the epicenter. Meanwhile, the number of NeuN immunoreactive neurons gradually decreased (P<0.05) from 0 mm to ±3 mm rostral and candual to the epicenter. Fourteen days after injury, the gray matter structure was no longer identifiable at the epicenter while the TUNEL-positive cells and NeuN immunoreactive neurons in the remaining anatomical positions remained at high levels. In rats that received methotrexate treatment, the number of NeuN immunoreactive neurons was significantly higher than those in model group (P<0.05, P<0.01). Conclusion: Low-dose methotrexate may decrease the nerve cell apoptosis via its metabolic product by exerting a protective effect on secondary injury of spinal cord.

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Influence of Chlorogenic Acid on Aβ_25-35-induced Damage to Granular Cell in Cerebellum

ZHOU Jing, ZHAO Hong, LIU Jian-sheng, YAO Su-yan, ZHENG De-yu

2013, 3 (6): 9-14.

Abstract ( 3093 )

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Objective: To investigate the effects of chlorogenic acid on granular cell in cerebellum induced by amyloid β- protein -induced macrophage activation in vitro. Methods: The experiment was divided into blank control group, Aβ_25-35 treatment group and Aβ_25-35+CHA co-processing of different time group; Blank control group: Equal amount of culture medium; Aβ_25-35 treatment group: with Aβ_25-3510 μmol·L^-1; Aβ_25-35and different time of CHA treatment group; The co-cultured system of cerebellar granular cells and macrophages were cultivated for 2 days and then the 10 μmol·L^-1 Aβ_25-35 and 1000 μmol·L^-1 CHA were added into this system for 6, 12, 24, 48, 96 h respectively. The growth phynotype of neurons and macrophages were detected by inverted phase contrast microscope; The expressions of p38MAPK, MAPKAPK-2, HSP27 protein were tested by Western blot. Results: The numbers cerebellar granule cell of chlorogenic acid protection group was increased significantly compared with Aβ_25-35 injury group. CHA could inhibite increased expression of phosphorylated p38MAPK of macrophage induced by Aβ_25-35 at difference time; Decreased expression of phosphorylated MAPKAPK-2 and phosphorylated HSP-27of macrophage induced by Aβ_25-35 could increased after the 1000 μmol·L^-1 CHA added into the medium. Conclusion: The protection of Chlorogenic acid for cerebellar granular cells induced by Aβ_25-35 via inhibition the activation of p38MAPK signaling pathway, which decreased the expression of p38MAPK and increased the expression of MAPKAPK-2, HSP-27.

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A Model of Cerebral Ischemia Injury in Streptozotocin-Induced Diabetic Rats

YAN Miao, WANG Shi-rui, LI Mei

2013, 3 (6): 15-19.

Abstract ( 2895 )

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Objective: To establish a reliable model of focal cerebral ischemia injury in diabetic rats, and to explore the criteria for successful modeling. Methods: Forty healthy male SD rats were randomly divided into three groups: a normal sham-operation group, a normal cerebral ischemia-reperfusion injury group and a group of diabetes combined with cerebral ischemia-reperfusion injury. Type I diabetes was induced by an intraperitoneal injection of streptozotocin (STZ, 60 mg·kg^-1). The body mass and the level of fasting blood glucose in each group were measured on Weeks 1 and 4 after STZ injection. A focal cerebral ischemia-reperfusion model was prepared by a thread occlusion method four weeks after STZ treatment. The scores of neurological function were assessed and the percentage of infarct volume were calculated after 30 min ischemia followed by 24 h of reperfusion. Results: The body mass (P<0.001) was reduced and the fasting blood glucose (P<0.001) was increased significantly in diabetic rats than those in normal rats four weeks after STZ injection. The percentage of infarct volume (P<0.001) was increased more significantly and the brain injury appeared more severe in diabetic rats than in normal rats after reperfusion. The success rate of this model was 73%. Conclusion: In this study, we developed a model of focal cerebral ischemia injury in diabetic rats that demonstrates a high success rate and good reliability and stability.

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Repairment of In Vitro Induced Neuron-like Cells on the Brain Injury in Rats

WEI Hui-ping, ZHU Deng- xiang, ZHANG Ai-lan, SONG Xiao-qing, CUI Le

2013, 3 (6): 20-24.

Abstract ( 2736 )

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Objective: To investigate the effect of neuron-like cells induced from bone marrow mesenchymal stem cells (BMSC) inthe repairment of brain injury in rats. Methods: BMSCs were isolated and cultured from rat's bone marrow by adherent method, identified by flow cytometry. BMSCs were induced into neuron-like cells using ligustrazine. 24 hrs after Neuron-like cell induction, the cells were directly transplanted into the hippocampus of rats with brain injury, and the survival of neuron-like cells in microenvironment of nervous system and pathological changes was examined. Results: Compared to rats with brain injury alone, rats that received neuron-like cells transplantation showed a decreased number of nerve cell degeneration and necrosis and less significant interstitial edema. Conclusion: rats with brain injury.Neuron-like cells induced from BMSC can improve brain function of

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Progress in the Relationship of Adult Hippocampal Neurogenesis and Alzheime’s Disease

HE Na, YIN Ming, WANG Ze-jian

2013, 3 (6): 25-32.

Abstract ( 2863 )

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Neurogenesis occurs throughout the adulthood in mammals, which involves neural stem cell proliferation, migration, differentiation and integration into the circuits. Alzheimer's disease (AD) is a progressive neurodegenerative disorder, characterized in the brain by amyloid plaque deposits, neurofibrillary tangles and neuronal loss. In recent years, evidence indicates that adult hippocampal neurogenesis provides new opportunities for the treatment for AD. Here we review recent progress on the relationship between adult hippocampal neurogenesis and AD.

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A Review on the Pharmacological Effects and Mechanisms of Osthole

ZHENG Li-qing, ZHANG Li, DONG Xiao-hua, WANG Jin

2013, 3 (6): 33-39.

Abstract ( 3197 )

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According to research status，this review summarized our current understanding of the pharmacological effects of that covers literature in the past 20 years. The pharmacological effects of osthole are wide, and may have value to develop into medications for the treatment of some disorders.

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Non-motor Symptoms of Parkinson’s Disease

WANG Jin

2013, 3 (6): 44-47.

Abstract ( 630 )

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Parkinson’s disease (PD) is a progressive，disabling neurodegenerative disorder with onset of motor and non-motor features. Non-motor symptoms include sleep disorders，neuropsychiatric symptoms，cognitive impairment，autonomic dysfunction，gastrointestinal and sensory symptoms. These symptoms are important factors related quality of life affected PD patients. This article will provide an overview of the non-motor symptoms of PD and their treatment options.

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The Correlation of General Anesthetic and Memory

WU Miao-miao, LI Wei, DONG Xiao-hua, ZHANG Dan-shen

2013, 3 (6): 48-56.

Abstract ( 3015 )

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General anesthetics are a class of drugs that have the ability to induce loss of consciousness and feeling, muscle relaxation and memory blockade, by reversibly inhibiting the central nervous system. Anesthetics target different receptors and brain regions to modify the various forms of memory. There are some patients with amnesia or even postoperative cognitive dysfunction. The effects of general anesthesia on memory seem to be related to the types of memory, age of the experimental subjects, the species and doses of the drug, and the types of the surgery. The underlying cellular substrates include γ-aminobutyric acid subtype A receptor, excitatory amino acid and synaptic plasticity.

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Review on Synaptic Plasticity Related Proteins

GUO Min, LI Gang

2013, 3 (6): 57-64.

Abstract ( 4023 )

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Synaptic plasticity is not only the molecular basis of learning and memory，but also the molecular mechanisms of signal transduction in the nervous system diseases. The synapses is a sensitive parts in synaptic plasticity，presynaptic and postsynaptic membrane accumulate many signal molecules that can lead to synaptic plasticity regulation. These molecules are very necessary for nerve transmission in synaptic parts. Recently, the research on the mechanisms of synaptic plasticity is mainly focus on the function of the presynaptic and postsynaptic related proteins and the nerve cytoskeletal proteins in signal pathway. Here is to review the latest progress in the synaptic plasticity related proteins.

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