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26 August 2013, Volume 3 Issue 4 Previous IssueNext Issue

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Effects of Morroniside on the expression of CyclinD1 and Cdk6 in Hippocampus of Rats with Focal Cerebral Ischemia/Reperfusion Injury LIU Ting-ting, SUN Fang-ling, AI Hou-xi, ZHANG Li, WANG Wen 2013, 3 (4): 1-7. Abstract( 2298) PDF(8380KB) ( 839) Objective: To explore the effects of morroniside on key cell-cycle regulator proteins in a rat model of focal cerebral ischemia-reperfusion. Methods: After the model of middle cerebral artery occlusion (MCAO) was established, 15 Sprague-Dawley rats were randomly assigned into sham group, model group, morroniside low dose (30 mg·kg-1) group, morroniside middle dose (90 mg·kg-1) group and morroniside high dose (270 mg·kg-1) group. Immunohistochemistry staining was used to measure the expression of CyclinD1 and Cdk6 in ischemic ipsilateral hippocampus. Results:Compared with sham group, the expression of CyclinD1 and Cdk6 were significantly increased in vehicle-treated ischemic-reperfusion rats. However, the expression of CyclinD1 and Cdk6 was significantly reduced by treatment of morroniside at doses of 90 mg·kg-1 and 270 mg·kg-1 after ischemia-reperfusion. Conclusion: Morroniside might play a role of neuroprotection by downregulating the expression of CyclinD1 and Cdk6 after cerebral ischemia-reperfusion. References|Related Articles|Metrics

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Effects of Emodin on Exploratory and Cognitive Function of Mice Experiencing Cerebral Ischemia Reperfusion WANG Shu, ZHANG Hai-hong, XUE Gui-ping 2013, 3 (4): 8-13. Abstract( 2043) PDF(1294KB) ( 1167) Objective: To study the effects and mechanisms of emodin on exploratory and cognitive functions of mice experiencing cerebral ischemia reperfusion. Methods: Using improved Himori method, cerebral ischemia reperfusion injury was produced in conscious mice by temporarily obstructing bilateral common carotid arteries. Effects of emodin (10.0, 1.0, 0.1 mg.kg-1，ip) on exploratory and cognitive function of mice experiencing cerebral ischemia reperfusion were assessed using the exploratory movement test and the step-through and step-down tests. The content of nitric oxide (NO) and the nitric oxide synthase (NOS) activities in brain and plasma, the content of hydrogen peroxide (H2O2) and catalase (CAT) activities in brain, and brain index were also measured. Results:Emodin significantly improved the exploratory and cognitive impairment induced by cerebral ischemia reperfusion injury, reduced the content of NO and H2O2, decreased the activities of NOS, and increased the activities of CAT and brain index. Conclusions: Emodin improved the performance in tests assessing exploratory and cognitive functions in mice experiencing cerebral ischemia reperfusion injury. Possible mechanisms include the reduction of the activities of NOS and enhancement of the activities of CAT, and clearance of the oxygen free radicals. References|Related Articles|Metrics

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Overview of the Pathogenesis and Animal Models of Alzheimer's Disease LIU Hong-bin，WU Hai-xia 2013, 3 (4): 14-22. Abstract( 2058) PDF(2497KB) ( 1492) Alzheimer's disease (AD) is a common neurodegenerative disease. The pathogenesis of AD is yet unclear and there is no satisfactory therapy for AD. AD transgenic models not only help to elucidate the pathogenesis of AD, but also provide potential screening models for drugs to treat the disease. At present, transgenic models have been regard as superior models for AD. In this review, we summarize the recent research progress on the pathogenesis of AD and transgenic models. References|Related Articles|Metrics

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Animal Models of Ulcerative Colitis: a Review WANG Qian, TIAN Hui, ZHANG Li 2013, 3 (4): 23-28. Abstract( 2299) PDF(1147KB) ( 2121) Ulcerative colitis (UC) is also known as chronic nonspecific ulcerative colitis. Epidemiological data suggest that the incidence of ulcerative colitis both in domestic and abroad has increased annually, thus attracting increasing research attention. Establishing valid animal models of ulcerative colitis seems particularly critical. In this review, animal models of ulcerative colitis were reviewed in the hope to provide guidance for related basic and clinical research. References|Related Articles|Metrics

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Research Progress of the Neroprotective Mechanism of Ischemic Postconditionining PU Ju, YAO Sheng-tao 2013, 3 (4): 29-34. Abstract( 1931) PDF(1103KB) ( 1291) Extending the thrombolysis time window and reducing reperfusion injury are problems urgently needed to be solved in ischemic cerebrovascular disease. Ischemic postconditioning provides a possible solution, which has been becoming a hot research topic. Postconditioning, which refers to a series of brief occlusions and reperfusions of the blood vessels, is conducted after ischemia/reperfusion. Postconditioning can induce organ's endogenous protective effects against ischemia reperfusion injury. This article will discuss the neuroprotective mechanism of ischemic postconditioning: reduction of brain blood flow changes after ischemia reperfusion, attenuation of ROS production and apoptosis, anti-inflammatory, and changes in pathways involved in neuronal death after stroke. References|Related Articles|Metrics

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Progress on the Correlation between Lead Poisoning and the Pathogenesis of Alzheimer’s Disease ZHANG Ji, WANG Shu, HOU Yong 2013, 3 (4): 35-38. Abstract( 2058) PDF(1064KB) ( 1008) Alzheimer's disease is a neurodegenerative disorder with unknown etiology, with senile plaques and neurofibrillary tangles as the main pathological features. In recent years, research on its pathogenesis and etiology has found some relationships between metal elements in the environment, such as lead, aluminum, copper etc. Alzheimer's disease, among which lead poisoning has become a hot topic. Research has also found a correlation between lead, neurotoxicity and lipid peroxidation. This review summarized recent research progress between the pathogenesis of lead poisoning and Alzheimer's disease. References|Related Articles|Metrics

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Anesthetic Mechanism, Its Protective Effect and Ion Channels LI Ying-jie，YANG Bao-xue 2013, 3 (4): 39-46. Abstract( 2237) PDF(1164KB) ( 1247) Anesthetics have been widely used in clinical surgeries, but their detailed mechanisms are still unclear. With the application of some new techniques, it is found that the ion channels are involved in anesthetic mechanisms, such as the suppression of N-methyl-D-aspartate channel and neuronal nicotinic acetylcholine receptors, inhibition of opening the voltage-gated ion channels function, and enhancing the GABAA-R channels. In addition, the protective effects of anesthetics on organs are also related with ion channels, which can be realized via activating potassium channels, attenuating calcium influx and so on. This article reviews the relationship between the anesthetics and ion channels in these two aspects. References|Related Articles|Metrics

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Review on the Impact of Rapid Eye Movement Sleep Deprivation on Synaptic Plasticity and its Molecular Mechanisms LI Wei，LI Ting-ting，QI Sai-qing，ZHANG Gui-rong 2013, 3 (4): 47-57. Abstract( 1942) PDF(1157KB) ( 1234) Insufficient sleep is an increasing serious problem to men and women in fast-paced modern society. Long-term insufficient sleep can lead to cognitive dysfunction. It has been widely recognized that sleep deprivation can affect the learning and memory ability of experimental animals. In this review, we summarized the new developments regarding the impact of rapid eye movement sleep deprivation on synaptic plasticity and its molecular mechanisms in recent years, which we hope can provide some basis for relevant studies of therapeutic targets and treatment drugs in future studies. References|Related Articles|Metrics

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An Update on Neuroprotective Effects of Estrogen in Alzheimer's Disease LIU Liang-jing, SHEN Li-xia 2013, 3 (4): 58-64. Abstract( 1854) PDF(1242KB) ( 1092) Alzheimer's disease is a disease caused by a variety of CNS-degenerating factors, characterized by deposition of amyloid beta and hyperphosphorylation of tau protein. Estrogen can inhibit neuronal cell apoptosis by inhibiting the activity of caspase, regulating of Bax and Bcl-2 expression and the ratio, increasing the content of cAMP in hypothalamic neurons and glial cells, promoting the rapid cAMP response element-binding protein (CREB) phosphorylation, influencing the N-methl-D-aspartate (NMDA) receptor expression in hippocampal cells. Estrogen also exerts direct protective effect on neuron cells by brain-derived neurotrophic factor and synaptophysin. Related Articles|Metrics