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26 February 2016, Volume 6 Issue 1 Previous IssueNext Issue

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Dendrobium Nobile Polysaccharides Attenuate Learning and Memory Deficits Induced by Lipopolysaccharide in Rats WANG Li-na，GONG Qi-hai，LI Fei，WU Qin，SHI Jing-shan 2016, 6 (1): 1-8. Abstract( 1959) PDF(6818KB) ( 1258) Objective：To investigate the protective effects and potential mechanisms of Dendrobium nobile polysaccharides （DNP） from Dendrobium nobile Lindl. on learning and memory deficits induced by lipopolysaccharide （LPS）. Methods：Rats were orally treated with DNP（ 40，80，160 mg·kg-1） for 7 days，followed by bilateral intra-cerebroventricular injection of LPS （20 μg·rat-1） to induce learning and memory deficits. Rats were continued to receive DNP until the end of experiments. Morris water maze was used to test the abilities of spatial learning and memory. The neuronal injury in hippocampus was observed by hematoxylin-eosin staining. The mRNA and protein expressions of neuroinflammation-related genes and proteins in rats hippocampus were detected by real time RT-PCR and Western blot，respectively. Results：Compared to sham （saline-injected） rats，LPS significantly prolonged the escape latency in the navigation test and shortened the adjusted escape latency （P<0.01）. These learning and memory deficits were significantly improved by DNP treatment （P<0.01）. LPS injection caused neuronal injury in hippocampus，and increased the mRNA and protein expressions of TNF-α，IL-1β and TGF-β1 in rat hippocampus （P<0.01），which were suppressed by DNP treatments （P<0.05）. Conclusions：DNP could protect LPS-induced learning and memory deficits and neuronal injury in rats. The mechanisms appear to be due to the inhibition of LPS-elicited inflammatory responses in the hippocampus. References|Related Articles|Metrics

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Study on Dynamic Anti-oxidative Effects of Chrysophanol Lipidosome on Cerebral Ischemia-reperfusion Injury in Mice YAN Juan，ZHENG Mao-dong，CUI Yu-huan，WEI Yu-lei，TIAN Qing-qing，ZHANG Dan-shen 2016, 6 (1): 9-17. Abstract( 1989) PDF(3312KB) ( 827) Objective：To explore the dynamic anti-oxidative effects of chrysophanol lipidosome on cerebral ischemia-reperfusion injury in mice. Methods：Mice were subjected to middle cerebral artery occlusion by suture method，then they were randomly divided into the control group，sham group，model group，nimodipine group （1.0 mg·kg-1） and chrysophanol lipidosome treatment （10.0，5.0，0.5 mg·kg-1） groups. The control group，sham group，modelgroup were injected with normal saline （10 mL·kg-1，ip）. Chrysophanol lipidosome treatment groups intraperitoneally were injected with chrysophanol lipidosome （10.0，5.0，0.5 mg·kg-1） before cerebral ischemia one hour，once a day，then the mice were divided into 6 subgroups according to different reperfusion time points，3，6，12，24，48，72 hour. According to the different time points，neurological deficits，brain water content，infarct volume were determined；the activity of NOS，SOD，GSH-PX，the content of MDA，NO were determined by the kits methods. Results：Compared with sham group，in model group the neurological deficits，brain water content，infarct volume were increased （P<0.01）；the activity of NOS and the content of MDA，NO were increased；the activity of SOD and GSH-PX were reduced （P<0.01）. Chrysophanol lipidosome reduced the neurological deficits，brain water content，infarct volume，the content of MDA，NO，and activity of NOS，and elevated the activities of SOD，GSH-PX （P<0.05）. Conclusion：So the protective effect of chrysophanol lipidosome on cerebral ischemiareperfusion injury might be involved in its anti-oxidative. References|Related Articles|Metrics

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Antiproliferation Effects of 2’-bro-2-hydroxy-4,6,4’,5’-tetramethoxychalcone on Human Neuroblastoma SK-N-SH Cells LIU Jun-ju，FU Dong-jun，NIU Jin-bo，ZHANG Qi，ZHANG Yan-bing 2016, 6 (1): 18-24. DOI:10.3969/j.issn.2095-1396.2016.01.003 Abstract( 1777) PDF(2144KB) ( 929) Objective：We studied the anti-proliferation effects of 2’-bro-2-hydroxy-4，6，4’，5’-tetrametho-xychalcone（C30） on human neuroblastoma and its mechanism to provide preliminary experimental evidence for its potential application to the prevention and treatment of neuroblastoma. Methods：The antiproliferation effects of the compounds on tumor cells were detected by sulforhodamine B（SRB） assay. Cell cycle distributions were measured by flow cytometry. Cellular apoptosis was detected by Hoechst 33258 staining assay and flow cytometry. Results：C30 restrained the proliferative effect of SK-N-SH cells in a dose- and time- dependent manner. After treated with C30，the cell cycle of SK-N-SH was arrested in G1 phase. Hoechst 33258 staining and flow cytometry analysis revealed that petasin could induce apoptosis in SKN-SH cells. Conclusion：C30 can inhibit the proliferation of SK-N-SH，and the mechanism maybe related to changing cell cycle distribution and inducing apoptosis. References|Related Articles|Metrics

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A Review of Studies on Blood Brain Barrier in vitro Model QIN Xue-qing，YANG Zhi-hong，SUN Xiao-bo 2016, 6 (1): 25-34. DOI:10.3969/j.issn.2095-1396.2016.01.004 Abstract( 2062) PDF(1762KB) ( 1884) Blood brain barrier（BBB） is a dynamic physiological structure，which is composed of brain microvascular endothelial cells，astrocytes and pericytes，playing an important role in maintaining homeostasis in the central nervous system. In vitro experiment is the preferred alternative to the study of early central nervous system drugs screening，pathological and physiological mechanism because of high-throughput，efficient，sensitive，rapid，and accurate characteristics. This paper focuses on the types，compositions and application of in vitro models of BBB，reviews the domestic and foreign literatures，describes the classical models and introduces the latest advanced technology，provides a reference for central nervous system drugs screening and in vitro BBB mechanism research. References|Related Articles|Metrics

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Role of Nuclear Transcription Factor Nrf2 in Parkinson’s Disease ZHANG Mei-jin，WANG Sha-sha，ZHANG Zhao，CHEN Nai-hong，HU Jin-feng 2016, 6 (1): 35-40. DOI:10.3969/j.issn.2095-1396.2016.01.005 Abstract( 2052) PDF(937KB) ( 1532) Nuclear factor erythroid-2-realted factor 2 （Nrf2） is an important transcription factor for cells to mediate the resistance to oxidative stress. As a pivotal protective mechanism，it binds to antioxidant response element （ARE） to resist internal and external oxidative stress.Recent studies have shown that the Keap1-Nrf2-ARE signaling pathway plays an important neuroprotective role in patients with Parkinson’s disease. In this paper，the role and its underlying mechanisms of Nrf2 in the treatment of Parkinson’s disease（PD），as well as the latest research achievements targeting Nrf2 for PD are summarized. References|Related Articles|Metrics

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Mechanism of Action of Autophagy on the Cerebral Ischemia-Reperfusion Injury WANG Xiao-ru，AN Fang 2016, 6 (1): 41-48. DOI:10.3969/j.issn.2095-1396.2016.01.006 Abstract( 2249) PDF(959KB) ( 1551) Autophagy is a life phenomenon widely existing in eukaryotic cells and a special metabolic pathway of decomposition. It controls the degradation of protein and organelles and is essential for cell survival and tissue homeostasis. At present，autophagy has become a hot research topic in the field of biological medicine，and the studies have demonstrated the association with various diseases. To date，ischemic cerebral stroke responsible for human death and disability may cause the ischemia-reperfusion （I/R） injury，which is common and receives much more concern. This review states autophagy and its mechanisms on the I/R injury to provide the theoretical basis for further therapy on ischemic cerebrovascular disorder. References|Related Articles|Metrics

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The Multi-target Mechanism of CCL2/CCR2 Involved in Neuropathic Pain LI Li，ZHANG Hai-lin 2016, 6 (1): 49-57. DOI:10.3969/j.issn.2095-1396.2016.01.007 Abstract( 1986) PDF(1022KB) ( 1428) CCL2 is the first discovered human CC chemokine and a potent chemotactic factor for monocytes，which induces immunological and inflammatory response. CCL2 and its receptor CCR2 play a key role in development and maintainence of neuropathic pain. Study found that CCL2 can be produced by neurons，and CCL2 acts as a neuromodulator in the process of pain disorder. CCL2 is the common mediator of neuropathic pain，immunological and inflammatory response. CCL2 involves in neuropathic pain at different levels，including peripheral sensory afferent nerve，dorsal root ganglia and spinal cord，which facilitates pain transmission. CCL2/CCR2 regulates neuropathic pain based on the following mechanisms：①enhances current amplitude and levels of TRPV1 mRNA by upregulating PI3K/Akt pathway，②CCL2 selectively increases mRNA of Nav1.8 through activating PI3K/Akt pathway and enhancing amplitude of TTX-R current，③significantly decreases voltage dependent noninactivation potassium current （IK） in DRG neurons，and has different effects on potassium channel in DRG neurons from different NP animal models，④enhances NMDA and AMPA evoked currents in spinal cord neurons，and enhances their spontaneous excitatory postsynaptic currents （EPSCs），⑤there is a bidirectional regulation between opioid receptors and CCL2/CCR2，⑥CCL2 directly inhibits GABA current in neurons. References|Related Articles|Metrics

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Parkinson Associated DJ-1 Gene and Oxidative Stress LOU Yu-xia, ZHANG Zhao, WANG Zhen-zhen, JIANG Yi-na, ZHANG Yi, LI Lin, CHEN Nai-hong 2016, 6 (1): 58-64. DOI:10.3969/j.issn.2095-1396.2016.01.008 Abstract( 1717) PDF(915KB) ( 1354) Parkinson’s disease is characterized by the substantia nigra pars compacta dopaminergic neuron-specific death and the presence of eosinophilic inclusion bodies-Lewy bodies which’s main component is α- synuclein in residual neuronal. Recent studies show that oxidative stress is a leading cause of brain dopaminergic neuron-specific death. DJ-1 （Park7） gene is an autosomal recessive Parkinson’s disease related genes. DJ-1 protein has a strong antioxidant effect，mainly acts as identity of active oxygen scavenger，chaperones，signaling pathways regulating molecules to against the oxidative stress，thereby protecting dopamine neurons from damage. Both deletion and mutation of DJ-1 gene will cause the reduction of its anti-oxidative stress，resulting in neuronal death，and this situation may be rescued by overexpression of DJ-1 protein. Because of the important role of DJ-1 in the development and occurrence of Parkinson’s disease，the paper will expand on its review of new research，and discuss primarily from the relationship between DJ-1 and oxidative stress. References|Related Articles|Metrics