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26 October 2011, Volume 1 Issue 5 Previous IssueNext Issue
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Protective Effect of PPT and Ginsenoside-Re in MPP+-treated SH-SY5Y Cells LI Dong-wei, DOU De-qiang 2011, 1 (5): 1-7. Abstract( 4037) PDF(1227KB) ( 2410) Objective:To investigate the protective effect of PPT (protopanaxatriol group) and ginsenoside-Re on 1-methyl-4-phenylpyridinium ion (MPP+)-induced damage in SH-SY5Y（human dopaminergic neuroblastoma cell line）cells. Methods:SH-SY5Y cells were treated with different concentrations of PPT, ginsenoside-Re or MPP+ containing serum. MTT colorimetry was used to test the viability of the cells and the survival rates were calculated and analyzed. Results:Cells treated by either 5 µmol•L-1, 10 µmol•L-1 PPT or ginsenoside-Reshowed significantly higher viability as compared to control group (P<0.05). In addition, 10% PPT treated or ginsenoside-Remedicated serum treated groups showed similar protective effect. Conclusion:PPT and ginsenoside-Re have neuroprotective effects in a cell model of Parkinson’s disease MPP +-induced SH-SY5Y cell death, suggesting that both PPT and ginsenoside-Re may have anti-PD effect. References|Related Articles|Metrics

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Effects of estradiol on learning and memory in ovariectomized rats: relationship with the contents of amino acids in the cerebrum ZHANG Xia-wei, ZHANG Dan-shen, XUE Gui-ping, ZHAO Yi-jie, JIN Can 2011, 1 (5): 8-13. Abstract( 3909) PDF(985KB) ( 2538) Objective: To investigate the influence of estradiol on learning and memory and the content of amino acids in the cerebrum of ovariectomized rats. Methods: Adult female rats were treated daily with subcutaneous injection of estradiol (75, 300 μg•kg-1) between weeks 7 and 16 after ovariectomy (OVX) or sham operation. The learning and memory of the rats was tested by a Morris water maze task on week 15, after which they were sacrificed and the content of amino acids in the cerebrum measured with high performance liquid chromatography (HPLC). Results: The ability of learning and memory was significantly improved, and the content of glutamic acid and the ratio of glutamic acid to γ-aminobutyric acid （Glu/GABA） in prefrontal cortex and hippocampus of OVX group was significantly decreased as compared to those of sham group. In addition, the ability of learning and memory of estradiol（75 μg•kg-1）treated group was significantly improved and the content of Glu and Glu/GABA in prefrontal cortex and hippocampus were significantly increased as compared to those of OVX group. However, the Glu/GABA ratio remained unchanged in the hippocampus of estradiol (300 μg•kg-1) treated group as compared to that of OVX group; and the ability of learning and memory in these rats did not significantly improve. Conclusion: Estradiol (75 μg•kg-1) improves the ability of learning and memory in OVX rats, and the increased Glu/GABA ratio in hippocampus possibly contributes to such an effect. References|Related Articles|Metrics

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Anti-thrombotic Effect of Earthworm Lyophilized Powder for Injection LIANG Chao, LIU Dong-jie, GAO Rui-chen, HAN Li-min, QU Yi, SHEN Xin, ZHU Jiu-xin, HOUYun-long, QIAO Guo-fen 2011, 1 (5): 14-18. Abstract( 2657) PDF(900KB) ( 2401) Objective: To observe the anti-thrombus effects of Earthworm lyophilized powder for injection(ELPI). Methods: The SD rats were randomly divided into blank control, low dose ELPI, and high dose ELPI groups, as well as ShuXueTong injection as the positive control. The models of carotid artery thrombus were induced by thrombus formation instrument; 72 hours after successful model establishment saline solution (2 mL•kg-1), earthworm low dose solution (0.9 mg•kg-1), earthworm high dose solution (1.8 mg•kg-1), and ShuXueTong solution (0.1 mL•kg-1) were injected via tail vein for 12 consecutive days. Then the carotid artery thrombus were peeled off and weighed. Blood was sampled for plasma t-PA level determination via ELISA method, CT and RT values were measured in all groups, and the maximal platelet aggregation rate was (PagR-max) was tested via LBY-NJ4 method. Results: Compared with the control group, thrombus weights in earthworm high dose group decreased significantly (P < 0.05); plasma t-PA levels in both low dose and positive control groups were significantly improved (P < 0.05); CT and RT in positive control and high-dose groups were significantly prolonged (P < 0.05), RT in low dose group also prolonged (P < 0.05), and this RT prolongation induced by ELPI was dose-dependent. Conclusion: ELPI possesses significant thrombolytic effects after 72 hours administration, and can inhibit intrinsic coagulation pathway through increasing plasma level of t-PA. References|Related Articles|Metrics

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The Effects of Stem-leaf Total Flavonoid on the Apoptosis Protein Expression and Ultrastructural Changes of Ischemia Reperfusion Damaged Neuron ZHAO Shu-min, KONG Wei, ZHANG Shu-feng, CHEN Meng, ZHENG Xiao-ying, KONG Xiang-yu 2011, 1 (5): 19-26. Abstract( 3695) PDF(1426KB) ( 2127) Objective: To investigate the protective effect of Scutellaria baicalensis Stem-leaf Total Flavonoid on ischemia reperfusion damaged neurons in rats and its mechanism. Methods: the rat model of focal ischemia reperfusion was prepared after pretreatment with different doses of SSTF. The neurological function deficit was evaluated according to the Zea Longa 5-grade marking system; the brain infarction volume was measured by Triphenytetrazolium chloride（TTC）staining methods, while the immunohistochemical method was used to detect brain neuronal apoptotic gene expression. The ultrastructural damage changes of the cerebral neurons were observed under the electron microscope. Results: The neurological function deficit was alleviated by different doses of SSTF, with the Bcl-2 protein expression up-regulated and Bax expression down-regulated. The damage of organelles, especially the mitochondria of the neuron was significantly reduced. Conclusions: SSTF pretreatment can alleviate the neuronal damage incurred by ischemia reperfusion, demonstrating neuroprotective effect. The mechanism of such a neuroprotection may involve prohibition of the apoptosis of the neurons. References|Related Articles|Metrics

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Paraquat-induced Neuronal Apoptosis Associated with Parkinson's Disease TIAN Xiao-fei, LI Jian-feng, PANG Hao 2011, 1 (5): 27-33. Abstract( 3664) PDF(932KB) ( 2149) Parkinson’s disease (PD) is a neurodegenerative disorder characterized by selective loss of dopaminergic neurons in the substantia nigra (SN); however, the causes of PD remain unknown. Over the years the etiologic involvement of genetic inheritance versus environmental exposures has been under debate. In this sense, a lack of evidence for heritability of the idiopathic PD has pointed to environmental risk factors as potential contributors to the disease etiology. It is reported that, Paraquat (PQ) (1,1-dimethyl-4,4′-bipyridinium dichloride), a widely used herbicide, was suggested as a potential etiologic factor for the development of PD. Paraquat is structurally similar to the neurotoxin MPP+ (1-methyl-4-phenylpyridinium), the latter being an active metabolite derived from MPTP (1- methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and being capable of inducing the apoptosis of neural cells. In this paper, we used the model of PQ induced toxicity on SH-SY5Y to study the mechanism underlying its effect in causing dopaminergic cells degeneration and necrosis. To this end, we determined whether PQ activated apoptotic pathways leading to the pathogenesis of PD as MPP+ does, or caused intracellular oxidative stress， mitochondrial dysfunction or proteasome abnormality to induce PD. Intensive study of the molecular mechanisms for PQ induction of PD will be of great value for the prevention and treatment of PD. References|Related Articles|Metrics

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The Mechanisms and Research Progress of Tau Abnormality Leading to AD Related Neurodegenerative Taupathies LI Li-xuan, LI Xiao-hui 2011, 1 (5): 34-39. Abstract( 4216) PDF(704KB) ( 2929) Tau, as a neuronally specific microtubule associated protein, plays a key role in promoting tubulin associated microtubule assembly, sustaining normal neuron axonal transport and stabilizing microtubule structure. Previous studies in autopsy revealed a tangible parallel relationship of brain neurofibrillary tangles (NFTs) to neurodegeneration, cell dysmorphology and apoptosis, thus leading to the consensus of NFTs being the major pathogenic factor in neurodegenerative taupathies, which are related to tau protein hyperphosphorylation. However, recent discoveries showed that Tau phosphorylation alone is insufficient for the formation of NFTs; other post-translational modifications such as glycosylation, proline isomerization, ubiquitination, as well as tau gene mutation and autophagy inhibition, are also required. In particular, recent researches using transgenic animals and multiphoton imaging technology indicated that NFTs seem to be just one clinical manifestation at the advanced stage of this disease, whereas soluble Tau protein plays an important role in initiating downstream pathological processes. Remarkably, suppression of Tau prohibited Aβ induced neuronal apoptosis and reduced memory impairment, suggesting that Aβ toxicity is Tau protein dependent. Along with the recent new light shed on the Tau abnormality induced neurodegenerative taupathies and its mechanism, Aβ as a drug target proved to be a failure in the field of drug discovery. As a result increasing attention has been given to tau targeted drug development. References|Related Articles|Metrics

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Distinct Roles and Modulations of Synaptic and Extrasynaptic NMDA Receptors CHU Shi-feng, CHEN Nai-hong 2011, 1 (5): 40-48. Abstract( 8354) PDF(790KB) ( 4515) N-Methyl-D-Aspartate receptor（NMDA receptor） has been considered as a double-edged sword in central nervous system. On the one hand, it mediates the calcium influx, promotes the synaptic plasticity and improves the neural excitatory. On the other hand, excessive opening of NMDA receptor causes calcium overload in neurons, disturbing the homeostasis and inducing the apoptosis. However, growing number of studies demonstrated that the distinct roles of NMDA receptor do not totally depend on its opening degree, but also on its locations where different signaling pathways are triggered. Synaptic NMDA receptors activate the nuclear calcium signaling pathways to protect the neurons; whereas activation of extrasyanptic NMDA receptor starts the apoptosis or death pathway. The imbalance between the two pathways accounts partially for pathogenesis in neural diseases, such as Alzheimer’s disease, Parkinson’s disease and Huntington’s disease. In conclusion, the currently available evidence has provided a new clue for the treatment of neurodegenerative disease. References|Related Articles|Metrics

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Neuroprotective role of the Alpha 2-Adrenergic Agonist Dexmedetomidine in Ischemic Cerebrovascular Disease HU Min, HE Zhi 2011, 1 (5): 49-55. Abstract( 5148) PDF(714KB) ( 3442) Ischemic cerebrovascular disease is a common and frequently encountered disease with high disability and mortality rates, and has severe effects on human’s health and quality of life. Cerebral hypoxic ischemia leads to an increase in the number of damaged or dead neurons. Recent studies have provided considerable evidence that alpha 2-adrenergic agonists can protect the brain neuron from cerebral ischemia/reperfusion injury. However, the exact mechanisms of this protection remain unknown. Activation of the alpha 2-adrenergic receptor may be involved. Dexmedetomidine is a highly selective agonist of the alpha 2-adrenergic receptors with neuroprotective effects. This article reviews the pathophysiological process of ischemic cerebrovascular disease, the molecular pharmacology and the neuroprotective mechanisms of dexmedetomidine. References|Related Articles|Metrics

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Targeting Nitrosative Stress as a Therapeutic Strategy for Neurovascular Protection in Brain Ischemia HUANG Ji-yun, HAN Feng 2011, 1 (5): 56-64. Abstract( 4576) PDF(757KB) ( 3124) Reactive nitrogen species (RNS) are major mediators of nitrosative stress, which causes protein tyrosine nitration and subsequently facilitates the breakdown of the highly-structured cellular machinery as well as the activation of cell death cascade. This review focuses on peroxynitrite (ONOO-)–mediated nitrosative stress signaling, which is closely associated with endothelial cell injury, cerebral edema and neurovascular damage that disrupt microvascular integrity in stroke. Growing evidence indicates that targeting nitrosative stress may be an important strategy to prevent the vascular complications associated with stroke. References|Related Articles|Metrics