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15 February 2012, Volume 7 Issue 5 Previous Issue    Next Issue

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Gastrodin inhibits neuroinflammation in rotenone-induced Parkinson’s disease model rats Chun Li, Xin Chen, Nan Zhang, Yangwen Song, Yang Mu 2012, 7 (5):  325-331.  Abstract ( 371 )   PDF (617KB) ( 1111 )   Save The present study showed that the latency of rats moving on a vertical grid was significantly prolonged, and the number of rats sliding down from the declined plane was increased remarkably, in rotenone-induced Parkinson’s disease model rats compared with control rats. The moving latency recovered to normal levels, but the number of slides was significantly increased at 28 days after model establishment. The slope test is a meaningful approach to evaluate the symptoms of Parkinson’s disease model rats treated with rotenone. In addition, loss of substantia nigral dopaminergic neurons in model rats was observed at 1 day after the model was established, and continued gradually at 14 and 28 days. The expression of tyrosine hydroxylase-positive cells was significantly increased in gastrodin-treated rats at 14 days. Significant numbers of activated microglia cells were observed in model rats at 14 and 28 days; treatment of rats with Madopar at 28 days suppressed microglial activation. Treatment of rats with gastrodin or Madopar at 28 days significantly reduced interleukin-1β expression. The loss of substantia nigral dopaminergic neurons paralleled the microglial activation in Parkinson’s disease model rats treated with rotenone. The inflammatory factors tumor necrosis factor-α and interleukin-1β are involved in the substantia nigral damage. Gastrodin could protect dopaminergic neurons via inhibition of interleukin-1β expression and neuroinflammation in the substantia nigra. Related Articles | Metrics

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Analysis of hippocampal gene expression profile of Alzheimer’s disease model rats using genome chip bioinformatics Yinghong Li, Zhengzhi Wu, Yu Jin, Anmin Wu, Meiqun Cao, Kehuan Sun, Xiuqin Jia, Manyin Chen 2012, 7 (5):  332-340.  Abstract ( 189 )   PDF (284KB) ( 1336 )   Save In this study, an Alzheimer’s disease model was established in rats through stereotactic injection of condensed amyloid beta 1-40 into the bilateral hippocampus, and the changes of gene expression profile in the hippocampus of rat models and sham-operated rats were compared by genome expression profiling analysis. Results showed that the expression of 50 genes was significantly up-regulated (fold change ≥ 2), while 21 genes were significantly down-regulated in the hippocampus of Alzheimer’s disease model rats (fold change ≤ 0.5) compared with the sham-operation group. The differentially expressed genes are involved in many functions, such as brain nerve system development, neuronal differentiation and functional regulation, cellular growth, differentiation and apoptosis, synaptogenesis and plasticity, inflammatory and immune responses, ion channels/transporters, signal transduction, cell material/energy metabolism. Our findings indicate that several genes were abnormally expressed in the metabolic and signal transduction pathways in the hippocampus of amyloid beta 1-40-induced rat model of Alzheimer’s disease, thereby affecting the hippocampal and brain functions. Related Articles | Metrics

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Two memory associated genes regulated by amyloid precursor protein intracellular domain Novel insights into the pathogenesis of learning and memory impairment in Alzheimer’s disease Chuandong Zheng, Xi Gu, Zhimei Zhong, Rui Zhu, Tianming Gao, Fang Wang 2012, 7 (5):  341-346.  Abstract ( 197 )   PDF (251KB) ( 806 )   Save In this study, we employed chromatin immunoprecipitation, a useful method for studying the locations of transcription factors bound to specific DNA regions in specific cells, to investigate amyloid precursor protein intracellular domain binding sites in chromatin DNA from hippocampal neurons of rats, and to screen out five putative genes associated with the learning and memory functions. The promoter regions of the calcium/calmodulin-dependent protein kinase II alpha and glutamate receptor-2 genes were amplified by PCR from DNA products immunoprecipitated by amyloid precursor protein intracellular domain. An electrophoretic mobility shift assay and western blot analysis suggested that the promoter regions of these two genes associated with learning and memory were bound by amyloid precursor protein intracellular domain (in complex form). Our experimental findings indicate that the amyloid precursor protein intracellular domain is involved in the transcriptional regulation of learning- and memory-associated genes in hippocampal neurons. These data may provide new insights into the molecular mechanism underlying the symptoms of progressive memory loss in Alzheimer’s disease. Related Articles | Metrics

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Brain-derived neurotrophic factor prevents beta- amyloid-induced apoptosis of pheochromocytoma cells by regulating Bax/Bcl-2 expression Zhikun Sun, Xingrong Ma, Hongqi Yang, Jiahua Zhao, Jiewen Zhang 2012, 7 (5):  347-351.  Abstract ( 201 )   PDF (210KB) ( 1046 )   Save Brain-derived neurotrophic factor was utilized in the present study to treat cell injury models induced by aggregated β-amyloid(25-35). Methylthiazolyldiphenyl-tetrazolium bromide assay and western blot analysis showed that brain-derived neurotrophic factor provided neuroprotection against cellular apoptosis by suppressing the decline in β-amyloid(25-35)-induced cell activity and the increasing ratio of Bax/Bcl-2. After treating pheochromocytoma cells with tyrosine kinase receptor B receptor inhibitor K252a, brain-derived neurotrophic factor reverses the above- mentioned changes. The experimental findings suggested that brain-derived neurotrophic factor prevented β-amyloid peptide-induced cellular apoptosis by modulating Bax/Bcl-2 expression, and this effect was associated with binding to the specific tyrosine kinase receptor B receptor. Related Articles | Metrics

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Long-term anodal block stimulation at sacral anterior roots promoted recovery of neurogenic bladder function in a rabbit model of complete spinal cord injury Xiaoran Wang, Qi Gao, Xiaoyu Yang, Weihua Wang, Xinquan Gu, Guifeng Liu, Peng Yan, Ge Gao, Xin Yu, Yongjie Wang, Jihu Lian, Chaoling Shi, Yao Wang, Li Fan 2012, 7 (5):  352-358.  Abstract ( 215 )   PDF (590KB) ( 993 )   Save A complete spinal cord injury model was established in experimental rabbits using the spinal cord clip compression method. Urodynamic examination was performed 2 weeks later to determine neurogenic bladder status. The rabbits were treated with anodal block stimulation at sacral anterior roots for 4 weeks. Electrical stimulation of sacral anterior roots improved urodynamic parameters of neurogenic bladder in rabbit models of complete spinal cord injury, effectively promoted urinary function, and relieved urinary retention. Immunohistochemistry results showed that a balance was achieved among expression of muscarinic receptor subunits M2, M3, ATP-gated ion channel P2X3 receptors, and β2-adrenergic receptor, and nerve growth factor expression decreased. These results suggested that long-term sacral anterior root stimulation of anodal block could be used to treat neurogenic bladder in a rabbit model of complete spinal cord injury. Related Articles | Metrics

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NG2 expression in rats with acute T10 spinal cord injury Haoran Lv, Jinshun Yang, Zhuangwen Liao, Yu Zhao, Yan Huang 2012, 7 (5):  359-362.  Abstract ( 227 )   PDF (219KB) ( 850 )   Save Rat models of T10 spinal cord injury were established with a clamp method. NG2 expression was detected with immunohistochemical staining and western blot. Ten days after spinal cord injury, the number of NG2-positive cells in the damaged areas and NG2 absorbance were both significantly increased. The findings indicate that acute T10 spinal cord injury in rats can lead to upregulation of NG2 protein expression in damaged areas. Related Articles | Metrics

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Fluoro-ruby retrograde tracing and three- dimensional visualization of the corticospinal tract in the guinea pig Xiao Han, Lulian Xu, Yue Wu, Hua Xun, Jinxiu Pan, Yingying Huang, Dafeng Ji, Huiqun Wu, Guangming Lv, Lemin Tang 2012, 7 (5):  363-367.  Abstract ( 208 )   PDF (196KB) ( 977 )   Save Fluoro-ruby was injected into the posterior funiculus of the spinal cord in the cervical (C5-T2) and lumbar (L3-6) segments of adult guinea pigs. The spinal cord was cut into serial frozen sections. The Fluoro-ruby labeling was clearly delineated from the surrounding structure. The labeling traversed the cervical, thoracic and lumbar segments, and was located on the ventral portion of the posterior funiculus on the injected side, proximal to the intermediate zone of the dorsal gray matter. The fluorescence area narrowed rostro-caudally. The spinal cord, spinal cord gray matter and corticospinal tract were reconstructed using 3D-DOCTOR 4.0 software, resulting in a robust three-dimensional profile. Using functionality provided by the reconstruction software, free multi-angle observation and sectioning could be conducted on the spinal cord and corticospinal tract. Our experimental findings indicate that the Fluoro-ruby retrograde fluorescent tracing technique can accurately display the anatomical location of corticospinal tract in the guinea pig and that three-dimensional reconstruction software can be used to provide a three-dimensional image of the corticospinal tract. Related Articles | Metrics

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Protein expression of sensory and motor nerves Two-dimensional gel electrophoresis and mass spectrometry Zhiwu Ren, Yu Wang, Jiang Peng, Li Zhang, Wenjing Xu, Xiangdang Liang, Qing Zhao, Shibi Lu 2012, 7 (5):  369-375.  Abstract ( 222 )   PDF (277KB) ( 840 )   Save The present study utilized samples from bilateral motor branches of the femoral nerve, as well as saphenous nerves, ventral roots, and dorsal roots of the spinal cord, to detect differential protein expression using two-dimensional gel electrophoresis and nano ultra-high performance liquid chromatography electrospray ionization mass spectrometry tandem mass spectrometry techniques. A mass spectrum was identified using the Mascot search. Results revealed differential expression of 11 proteins, including transgelin, Ig kappa chain precursor, plasma glutathione peroxidase precursor, an unnamed protein product (gi|55628), glyceraldehyde-3-phosphate dehydrogenase-like protein, lactoylglutathione lyase, adenylate kinase isozyme 1, two unnamed proteins products (gi|55628 and gi|1334163), and poly(rC)-binding protein 1 in motor and sensory nerves. Results suggested that these proteins played roles in specific nerve regeneration following peripheral nerve injury and served as specific markers for motor and sensory nerves. Related Articles | Metrics

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Oxidative stress in neurodegenerative diseases Xueping Chen, Chunyan Guo, Jiming Kong 2012, 7 (5):  376-385.  Abstract ( 530 )   PDF (158KB) ( 1255 )   Save Reactive oxygen species are constantly produced in aerobic organisms as by-products of normal oxygen metabolism and include free radicals such as superoxide anion (O2−) and hydroxyl radical (OH−), and non-radical hydrogen peroxide (H2O2). The mitochondrial respiratory chain and enzymatic reactions by various enzymes are endogenous sources of reactive oxygen species. Exogenous reactive oxygen species -inducing stressors include ionizing radiation, ultraviolet light, and divergent oxidizing chemicals. At low concentrations, reactive oxygen species serve as an important second messenger in cell signaling; however, at higher concentrations and long-term exposure, reactive oxygen species can damage cellular macromolecules such as DNA, proteins, and lipids, which leads to necrotic and apoptotic cell death. Oxidative stress is a condition of imbalance between reactive oxygen species formation and cellular antioxidant capacity due to enhanced ROS generation and/or dysfunction of the antioxidant system. Biochemical alterations in these macromolecular components can lead to various pathological conditions and human diseases, especially neurodegenerative diseases. Neurodegenerative diseases are morphologically featured by progressive cell loss in specific vulnerable neuronal cells, often associated with cytoskeletal protein aggregates forming inclusions in neurons and/or glial cells. Deposition of abnormal aggregated proteins and disruption of metal ions homeostasis are highly associated with oxidative stress. The main aim of this review is to present as much detailed information as possible that is available on various neurodegenerative disorders and their connection with oxidative stress. A variety of therapeutic strategies designed to address these pathological processes are also described. For the future therapeutic direction, one specific pathway that involves the transcription factor nuclear factor erythroid 2-related factor 2 is receiving considerable attention. Related Articles | Metrics

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Neural plasticity after spinal cord injury Jian Liu, Xiaoyu Yang, Lianying Jiang, Chunxin Wang, Maoguang Yang 2012, 7 (5):  386-391.  Abstract ( 259 )   PDF (126KB) ( 1104 )   Save Plasticity changes of uninjured nerves can result in a novel neural circuit after spinal cord injury, which can restore sensory and motor functions to different degrees. Although processes of neural plasticity have been studied, the mechanism and treatment to effectively improve neural plasticity changes remain controversial. The present study reviewed studies regarding plasticity of the central nervous system and methods for promoting plasticity to improve repair of injured central nerves. The results showed that synaptic reorganization, axonal sprouting, and neurogenesis are critical factors for neural circuit reconstruction. Directed functional exercise, neurotrophic factor and transplantation of nerve-derived and non-nerve-derived tissues and cells can effectively ameliorate functional disturbances caused by spinal cord injury and improve quality of life for patients. Related Articles | Metrics

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Detrimental impact of hyperlipidemia on the peripheral nervous system A novel target of medical epidemiological and fundamental research study Song Wu, Xu Cao, Rongzhen He, Kun Xiong 2012, 7 (5):  392-399.  Abstract ( 200 )   PDF (146KB) ( 1620 )   Save Recently, epidemiological studies on the etiology of peripheral neuropathies have revealed that hyperlipidemia is a novel risk factor. Plasma lipid levels were confirmed to be associated with the incidence of many peripheral neuropathies including axonal distal polyneuropathy, vision and hearing loss, motor nerve system lesions and sympathetic nerve system dysfunction. Moreover, different lipid components such as cholesterol, triacylglycerols and lipoprotein are involved in the pathogenesis of these neuropathies. This review aimed to discuss the effect of hyperlipidemia on the peripheral nervous system and its association with peripheral neuropathies. Furthermore, a detailed discussion focusing on the explicit mechanisms related to hyperlipidemia-induced peripheral neuropathies is presented here. These mechanisms, including intracellular oxidative stress, inflammatory lesions, ischemia and dysregulation of local lipid metabolism, share pathways and interact mutually. In addition, we examined current information on clinical trials to prevent and treat peripheral neuropathies caused by hyperlipidemia, with a predictive discussion regarding the orientation of future investigations. Related Articles | Metrics