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26 August 2011, Volume 1 Issue 4 Previous Issue    Next Issue

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α-Synuclein Inhibits the Expression of BDNF in PC12 Cells YUAN Yu-he，WU Miao-miao，HU Jin-feng，CHEN Nai-hong 2011, 1 (4):  1-5.  Abstract ( 3811 )   PDF (3549KB) ( 2759 )   Objective：To research the effect of α-synuclein on the brain derived neurophic factor (BDNF) expression. Methods：Recombinant plasmids were constructed using molecular techniques and were used to transfect mammalian cells. The protein level was examined by western blotting assay and the activity of transcription factors was tested by dual-luciferase reporter assay system. Results：Overexpression of α-synuclein inhibited the expression of BDNF and attenuated the transcription activity of cAMP response element binding protein (CREB)，but did not affect the activity of Nurr1. Besides，CREB ser-133 phosphorylation level was decreased when α-synuclein was overexpressed. Conclusion：Overexpressed α-synuclein down-regulates BDNF probably through depressing the activities of CREB transcription factors. References | Related Articles | Metrics

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The Antidepressant Effect of the Total Flavonoids Extracted fromCottonseed and its Regulation on Hippocampal Monoamines ZHAO Nan，ZHANG You-zhi，YANG Ming，WANG Yi-wen，ZHAO Yi-min，GONG Ze-hui，LI Yun-feng 2011, 1 (4):  6-11.  Abstract ( 4263 )   PDF (1230KB) ( 2657 )   Objective：To explore the antidepressant effect of the total flavonoids extracted from cottonseed (CTN-T) and its possible mechanism. Methods：The learned helplessness model in rats was used to evaluate the antidepressant effect of CTN-T. Using the 5-hydroxytryptophan（5-HTP）induced head twitch response test and yohimbine toxicity potentiation test in mice，the possible monoamine targets of the antidepressant action of CTN-T were detected. Moreover， high performance liquid chromatography and electrochemical detection (HPLC-ECD) was used to determine the content of monoamine and metabolites in the hippocampus of rats following CTN-T administration. Results：Repeated administration of CTN-T (50，100 mg·kg-1，ig，twiceper day for 4 d) significantly decreased the helplessness behavior induced by inescapable foot- shock in learned helplessness test in rats. Repeated administration of CTN-T (50，75 mg·kg-1， ig，twice per day for 4 d) significantly increased the 5-HTP induced head twitch response in  mice，while CTN-T (60 mg·kg-1，ig，twice  per day for 4 d) had a tendency to potentiate yohimbine toxicity in mice. Repeated administration of CTN-T (25~75 mg·kg-1，ig，twice  per day for 4 d)，the neurochemical assays showed that the content of 5-hydroxytryptamine (5-HT) was increased in rat hippocampus at 25 and 100 mg·kg-1  dose of CTN-T，and that the content of norepinephrine (NE) was increased at 50 and 100 mg·kg-1  dose of CTN-T. By contrast，CTN-T had no effects on the content of dopamine (DA)，epinephrine (E)，5-hydroxyindolacetic acid (5-HIAA) and the rate of 5-HT/5-HIAA. Conclusion：CTN-T exerts antidepressant effects which may be closely related to the strengthening of the hippocampal serotonergic and noradrenergic function. References | Related Articles | Metrics

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Effects of Phillyrin on MPP+-induced Injury in SH-SY5Y Neuroblastoma Cells ZHANG Mei-rong, WEI Shou-rong, WU Yan-chuan, SUN Fang-ling, AI Hou-xi, ZHANG Li, WANG Wen 2011, 1 (4):  12-15.  Abstract ( 4244 )   PDF (1085KB) ( 3022 )   Objective：To investigate the effects of Phillyrin on 1-methyl-4-phenylpyridinium (MPP+) -induced injury in SH-SY5Y neuroblastoma cells. Methods：SH-SY5Y cells were incubated with Phillyrin of different concentrations. MTT metabolic rate was measured as the cell survival rate to determine the effective concentrations of Phillyrin. After SH-SY5Y cells were incubated with Phillyrin (1，10，100 μmol·L-1) for 24 h prior to exposure to MPP+ (1 mmol·L-1) for 48 h，the MTT metabolic rate and LDH leakage rate were observed. Results：Phillyrin did not decrease the survival rate of SH-SY5Y cells at the concentrations from 1 to 100 μmol·L-1. Compared with the control group，MPP+ decreased the MTT metabolic rate （P<0.001） and increased the LDH leakage rate (P<0.001) of SH-SY5Y cells. However，Phillyrin significantly increased the cell activity (P<0.05) and decreased LDH leakage rate of SH-SY5Y cells with MPP+-induced injury. Conclusion：Phillyrin protects SH-SY5Y cells against MPP+-induced cytotoxicity. References | Related Articles | Metrics

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Comparison in Tissue Distribution and Pharmacodynamics Effects between Three Chrysophanol Formulations in Mice with Cerebral Ischemia Reperfusion LI Chao, ZHANG Li 2011, 1 (4):  16-25.  Abstract ( 3454 )   PDF (2698KB) ( 2733 )   Objective：To compare the pharmacodynamics and the tissue distribution of chrysophanol loaded polybutylcyanoacrylate nanocapsules，chrysophanol-hydroxypropyl-β-cyclodextrin inclusion complex，chrysophanol liposomes and DMF dissolved chrysophanol in mice with cerebral ischemia reperfusion. Methods：Using the cerebral ischemia reperfusion injury model，determined the chrysophanol content in blood，brain，heart，kidney，liver，spleen，lung of mice；measured the activity of malondialdehyde (MDA)，monoamine oxidase-B (MAO-B)，nitric oxide (NO)，nitric oxide synthase (NOS)，lipofuscin (LF)，acetylcholinesterase (AChE) in brain，the content of amino acid (AA) in brain and the content of lipofuscin (LF) in heart；observed the morphology of hippocampal. Results：The order of chrysophanol concentration in mouse tissues is：blood>brain>kidney>liver>heart>spleen>lung. Compared with chrysophanol DMF，chrysophanol concentrations of chrysophanol formulations (10.0，1.0，0.1 mg·kg-1 dose groups) in brain，liver and blood tissues were significantly high (P<0.01~0.05) in a dose-dependent manner. At the same time，the aging-related enzymes’ activity and the pathological morphology in hippocampal area were improved to some extent. Conclusion：All the three chrysophanol formulations could enhance the anti-aging effects of chrysophanol in mice with cerebral ischemia reperfusion，with the possible mechanisms involving enhancement of chrysophanol content in brain，regulation of the activity of aging-related enzymes and improvement of the pathological morphology in hippocampi area. References | Related Articles | Metrics

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The Role of MicroRNA in Learning and Memory Dysfunction CHEHui, YANG Bao-feng, AIJing 2011, 1 (4):  26-32.  Abstract ( 4089 )   PDF (1098KB) ( 3188 )   MicroRNAs (miRNAs) are endogenous small RNAs that can silence the gene expression. miRNAs play an important role in neuronal development，differentiation and function. Neurodegenerative diseases and depression are associated with impairment of learning and memory. The deregulation of miRNAs can affect the occurrence and development of these diseases in many ways. This review highlights the effect of miRNAs on synaptic plasticity and diseases，and also discusses the function of miRNAs in learning and memory dysfunction. References | Related Articles | Metrics

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Research Progress on Hyperammonia-induced Hepatic Encepha-lopathy XUE Zhan-xia, PENG Liang 2011, 1 (4):  33-41.  Abstract ( 3967 )   PDF (1140KB) ( 2494 )   Hepatic encephalopathy （HE） is a serious complication of acute or chronic liver failure，caused by many reasons （i.e. ammonia，multiple neurotoxins，false neurotransmitters and benzodiazepine-like compounds）. Evidences suggest that ammonia plays a major role in pathogenesis of HE. Hyperammonia up-regulates gene expression of peripheral-type benzodiazepine receptor （PTBR），glucose tranporter-1 （GLUT-1），aquaporin-4 （AQP4），and Na+/K+-ATPase in astrocytes；alters the phosphorylation state of the microtubule-associated protein-2 （MAP-2） and the expression of N-methyl-D-aspartate （NMDA） receptor；induces increase of NO，therefore astrocytic disfunction. It was reported previously that ammonia increased production of ouabain-like compounds and Na+/K+-ATPase activity in astrocytes. Research to the relationship of these factors will help us to understand the underlying mechanisms of ammonia-induced astrocytic disfunction and eventually contribute to the new strategies of prevention and therapy of HE. References | Related Articles | Metrics

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Research Progress in the Mechanisms of Cerebral Ischemia Hypoxia Preconditioning Antagonizing Cerebral Ischemia and Hypoxia Injury YUAN Heng-jie，LOU Jian-shi 2011, 1 (4):  42-47.  Abstract ( 4121 )   PDF (1062KB) ( 2891 )   The phenomenona of ischemia/hypoxia preconditioning were first discovered in heart. Numerous studies，carried out at different levels，have confirmed that there are also preconditioning phenomenona in brain，and the phenomenona of ischemia/hypoxia preconditioning in brain have become a hot topic in the field of ischemia and hypoxia. Cerebral ischemia/hypoxia preconditioning (CIP) can decrease cell apoptosis，increase the anti-oxidant ability and decrease oxidant injury，increase the generation of hypoxic inducible factor-1 and heat shock protein 70 through multiple signal transduction pathways. There are interactions among the mechanisms about CIP which are relatively independent. References | Related Articles | Metrics

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Application Advances on Novel Techniques in Multi-target Drugs Discovery LIU Shao-qiang，TIE Lu，LI Xue-jun 2011, 1 (4):  48-54.  Abstract ( 3798 )   PDF (1049KB) ( 3219 )   Compared with drugs designed to act against individual molecular targets，multi-target drugs that impact multiple targets simultaneously are better at controlling complex disease systems and are less prone to drug resistance. However，how to design multi-target drugs presents a great challenge. With the rapid progress in multi-target drugs research，some novel techniques in laboratories have emerged and are very likely to be effectively applied in combating multigenic diseases or diseases that affect multiple tissues. This review deals with the recent progress in multi-target drugs research，some novel techniques and their applications in drug discovery. References | Related Articles | Metrics

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Research Advances in Using Ginseng to Prevent and Treat Parkinson’s Disease LI Dong-wei, DOU De-qiang 2011, 1 (4):  55-64.  Abstract ( 4909 )   PDF (1686KB) ( 3419 )   The current research in Parkinson’s disease and progress in using of ginseng to treat Parkinson’s disease，and mechanisms of ginsenosides-induced protection of dopaminergic neurons in substantia nigra were reviewed，which lay a foundation for the reasonable application of ginseng in the treatment of Parkinson’s disease. Ginsenosides can play an important role in protecting dopaminergic neurons by countering oxidative stress，inhibiting Ca2+ channel and blocking the signaling pathways of neurons apoptosis. References | Related Articles | Metrics