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    26 April 2011, Volume 1 Issue 2 Previous Issue    Next Issue

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    Rosiglitazone Improves Cognitive Impairment in Streptozotocin-induced Diabetic Mice and its Mechanisms
    ZHANG Ting-ting,LIU Li-ping,JIANG Li-ying,HU Wei,LONG Yan,HONG Hao
    2011, 1 (2):  1-6. 
    Abstract ( 5060 )   PDF (1263KB) ( 3083 )  
    Objective: To investigate the effects of rosiglitazone on cognitive function in streptozotocin-induced diabetic mice and the underlying mechanisms. Methods: Diabetic mice induced by a single intravenous injection of streptozotocin(150 mg• kg-1 body weigh)were used as animal model of type 1 diabetes. Diabetic mice with hyperglycemia(>11.1 mmol•L-1)were randomly divided into three groups,including untreated diabetes group, rosiglitazone( 3.2 mg•kg-1 and 1.6 mg•kg-1)treated groups(10~12 mice/group). After orally administration of rosiglitazone for 6 w, rosiglitazone-treated diabetic mice, untreated diabetic mice and non-diabetic controls were tested in the Morris water maze and Y maze. The serum insulin,the levels of Aβ40,Aβ42 and BACE1 in hippocampus and cortex were determined by ELISA assays,and the blood glucose was measured by the glucose oxidase method. Results: Both water maze and Y maze learning were impaired in diabetic mice. In Morris water maze, rosiglitazone(3.2 mg• kg-1)significantly decreased the escape latency(P<0.05)and increased the time spent in the platform quadran(P<0.05)compared with the vehicle diabetic group. Rosiglitazone(3.2 mg• kg-1)also significantly increased the number of correct(P<0.05)in Y maze test. Rosiglitazone treatment did not decrease the blood glucose and serum insulin of diabetic mice. Rosiglitazone(3.2 mg• kg-1)significantly decreased the Aβ40P<0.05, P<0.05)and Aβ42P<0.05, P<0.05)levels in both hippocampus and cerebral cortex of diabetic mice, without reducing the increased BACE1 level. Conclusion: Rosiglitazone at the dosage of 3.2 mg• kg-1 improves cognitive impairments in streptozotocin-induced diabetic mice via the alleviation of the Aβ burden in the brain.
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    Effects of Chrysophanol Liposomes on Apoptosis of the Hippocampal Neurons in Mice after Cerebral Ischemia and Reperfusion Injury
    SONG Jin-yan, ZHANG Li, ZHAO Xiao-qian, SONG Zhi-bin
    2011, 1 (2):  7-13. 
    Abstract ( 6376 )   PDF (1243KB) ( 2712 )  
    Objective: To observe the influence of chrysophanol liposomes on apoptosis of hippocampal neurons in mice and to study the protective effects on cerebral ischemia and reperfusion injury and its mechanism. Methods: Cerebral ischemia and reperfusion injury was produced in conscious mice by temporarily obstructing bilateral common carotid arteries. Chrysophanol liposomes(10.0,1.0,0.1 mg· kg-1)was injected intraperitoneally. The effects of chrysophanol liposomes were studied on the neurological function, the pathomorphology of brain tissues and the expression of apoptosisrelated protein caspase-3, Bcl-2 and Bax in hippocampal neuron using immunohistochemistry. Results: Chrysophanol liposomes could increase the expression of Bcl-2, decrease the expression of Bax and caspase-3, improve the neurological function score and decrease the pathological change in chrysophanol liposomes treated animals. The effect of chrysophanol liposomes was most obviously in group 10.0 mg· kg-1P<0.05). Conclusion: Chrysophanol liposomes have a significant protective effect on hippocampal neurons after cerebral ischemia and reperfusion injury. The mechanism may be related to increasing the expression of Bcl-2, reducing caspase-3 and Bax.
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    Effect of Scutellaria Baicalensis Stem-leaf Total Flavonoid on Learning and Memory Impairment Induced by Aβ25-35 and Activity of Anti-oxidative Enzyme of Hippocampus in Rats
    WANG Rui-ting, GUAN Li-hua, ZHOU Jian, SHEN Xing-bin,ZHANG Jian-xin
    2011, 1 (2):  14-18. 
    Abstract ( 4263 )   PDF (1188KB) ( 2718 )  
    Objective: To explore the effect of scutellaria baicalensis stem-leaf total flavonoid(SSTF)on learning and memory damage induced by Aβ25-35 and on the activity of anti-oxidative enzyme. Methods:Rats were administered SSTF(100,50,25 mg• kg-1,ig). The AD model was made by bilateral injection of Aβ25-35 in rat hippocampus. Morris water maze was used to evaluate the learning and memory ability of the rats. HE stain was used to observe morphology of the neuron of hippocampus CA1 region. The activity of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px)and the content of malondialdehyde(MDA)in rat hippocampus were measured. Results: Compared with that of the control group, the latency to find the platform in model group was significantly increased, and the ratio of path in platform quadrant to the whole path was significantly decreased. Compared with that of the model rats, the latency to find the platformin animals with SSTF 100,50 mg• kg-1 and vitamin E (Vit E)groups were significantly decreased, the ratio of path in platform quadrant to the whole path was significantly increased. The CA1 region neuron of the model rats showed severe damage. Compared with of the model rats, the neuron of SSTF and Vit E groups showed a decreased damage. Activities of SOD, GSH-Px in SSTF and Vit E group were significantly increased compared with that in the model rats. Content of MDA in SSTF and Vit E groups were significantly decreased compared with that in the model rats. Conclusion: SSTF can attenuate neuron damage and learning impairment induced by Aβ, and the mechanism may be related to the increased activity of anti-oxidative enzyme.
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    Changes of PTEN (Phosphatase and Tensin Homolog Deleted on Chromosome 10) Gene Level in the Hippocampus of Experimental Alzheimer’s Disease Mice
    XU Jian-wen, YANG Jian, YU Chang-xi
    2011, 1 (2):  19-23. 
    Abstract ( 4554 )   PDF (1498KB) ( 2796 )  
    Objective: To investigate the dynamic alteration of PTEN(Phosphatase and Tensin Homolog Deleted on Chromosome 10)and phospho-PTEN levels at different stages of mimic Alzheimer’s disease(AD)mice induced by AlCl3. Methods:AD-like mouse was made by intracere-broventricular injection(icv)of 2 μL of 0.5% AlCl3 dissolved in artificial cerebrospinal fluid, once a day, consecutively for 5 d. Passive avoidance response test was used at d 2 and d 7, and Morris water maze test at d 23 to d 30 after the last icv injection to detect the learning and memory capabilities of mice. Western Blotting was used to detect the protein levels of PTEN and phospho-PTEN in the hippocampus of mice. Results: The results of step through passive avoidance response showed a significant retardation of the model mice from d 2 to d 7 after the last icv injection compared with that of the control group; from d 23 to d 30 after the last icv injection, Morris water maze(MWM) performance displayed a significant impairment in learning and memory ability of model mice. No significant differences on protein levels of PTEN and phospho-PTEN in the hippocampus were found between the model mice and control mice at the d 2 and d 7 time-points after the last icv injection. At the d 30 time-point after the last icv injection, the protein level of phospho-PTEN-Ser380 of the model mice was significantly lower than that of the control group, but no significant difference about PTEN protein level. Conclusion:The phospho-PTEN protein level of hippocampus in the late development stage of mimic AD mice induced by aluminum toxicity is decreased significantly.
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    Production of Microencapsulated Human Retinal Pigment Epithelial Cells by the High Voltage Electrostatic Method
    GAO Dong-xiao,ZHAO Ya-qun
    2011, 1 (2):  24-27. 
    Abstract ( 3588 )   PDF (1237KB) ( 2891 )  
    Objective: To prepare alginate-chitosan-alginate(Alginate-Chitosan-Alginate, ACA) microencapsulated Human Retinal Pigment Epithelial(hRPE) cells using high voltage electrostatic method. Methods: The microencapsulated hRPE was prepared by using our home-made high voltage electrostatic system, and the total number and the survival rate of microencapsulated hRPE cells were studied in the culture media for 7 d. Results: hRPE cells ACA microcapsule with diameter of (400±13) μm were obtained. the total number and the survival rate of cells had no statistically significant differences at the first 3 d. But after 7 d the total number of cells and the survival number were increased and the survival rate of cells was reduced. Conclusion: hRPE cells ACA microcapsule can be obtained with high voltage electrostatic method; after 7 d, the microencapsulated cells grow faster.
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    Comparison of Sexual Hormone Levels and Hypothalamic Mitochondrial Aging in Two Rat Models of Menopausal Status
    GU Zu-xi, XU Lian-wei, SUN Zhuo-jun, LIU Jian-wen, LI Sheng-nan, MOU Yan-yan, ZHANG Huan-ying, ZHANG Ting-ting, SANG Zhen, MA Jun, LU Xiong
    2011, 1 (2):  28-34. 
    Abstract ( 4152 )   PDF (1427KB) ( 2915 )  
    Objective: To characterize 5-month-old ovariectomized and 18-month-old female rats as models for menopausal females. Methods: Sexual hormones FSH, LH and E2 were measured in serum and hypothalamus, and superoxide dismutase(SOD), malondialdehyde(MDA)and total anti-oxidative capacity(T-AOC)in hypothalamus of a total of 71 Sprague Dawley female rats of 4 groups: 5-month-old control group, 5-month-old ovariectomized model group, 18-months-old model group and 24-month-old aged control group. Mitochondria DNA damage was monitored by measuring expression level of mRNA of CoⅠ and CoⅢ using quantitative RT-PCR. Ultrastructure of mitochondria of hypothalamus neuron cells was investigated using transmission electron microscope. Results: Compared with 5-month-old control rats, FSH and LH increased and E2 decreased in serum and hypothalamus significantly(P<0.05)in both 5-month-old ovariectomized rats and 18-month-old rats. Antioxidants SOD and T-AOC of hypothalamus were reduced significantly in 5-month-old ova-riectomized rats and 18-month-old rats(P<0.01). The expression levels of CoⅠ and Co Ⅲ, indications of hypothalamus mitochondria DNA damage, were at lowest in 5-month-old controls rats followed by ovariectomized 5-month-old rats, 18-month-old rats and 24-month-old rats(P<0.001). Ultrastructural impairment of mitochondria of hypothalamic neuron cells was visible in both 5-month-old ovariecto-mized rats and 18-month-old rats. Conclusion: Both 5-month-old ovariectomied rats and 18-month-old rats have sexual hormones changes similar to that of menopausal females. Removal of bilateral ovaries in young rats not only lead to hormonal change but also results in mitochondria aging as 18-month-old rats have. Thus both 5-month-old ovariectomized rats and 18-month-old rats may mimic the status of sex endocrine change and hypothalamus aging in menopause females.
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    Methods and Evaluation of Animal Models of Induced Cough
    ZHANG Dan-shen
    2011, 1 (2):  35-41. 
    Abstract ( 4519 )   PDF (1062KB) ( 4091 )  
    The cough induced by many factors is a common symptom of a variety of respiratory diseases. Ideal animal models are needed not only for the studies on the incidence and control mechanisms of the cough reflex, and etiology and pathogenesis of the cough, but also for the research and development of effective antitussives and the treatment of human cough. In this review, the animal models of induced cough were described in detail and evaluated to provide some guidance for related basic and clinical research and applications.
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    Roles of Adenomatous Polyosis Coli in the Early Developing Cerebral Cortex
    ZUO Wei, JI Hui, WANG Wen
    2011, 1 (2):  42-47. 
    Abstract ( 4733 )   PDF (1009KB) ( 3579 )  
    Adenomatous polyosis coli(APC)is a large multifunctional protein known to be important for Wntβ-catenin signalling, cytoskeletal dynamics, and cell polarity. In the developing cerebral cortex, APC is expressed in proliferating cells and its expression increases as cells migrate to the cortical plate. In this article, we summarized the roles of APC in the early developing cerebral cortex. APC is required for multiple aspects of early cerebral cortical development, including the regulation of cell number, interkinetic nuclear migration, cell polarity, and cell type specification.
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    Research Progress on Pharmacologic Actions of Curcumin in Central Nervous System
    LI Gao-wen, XU Ying, KU Bao-shan, PAN Jian-chun
    2011, 1 (2):  48-57. 
    Abstract ( 6714 )   PDF (1221KB) ( 4535 )  
    Curcumin, an active yellow polyphenol pigment of turmeric, belongs to polyphone compound. Quantities of research have proved its pharmacologic actions in peripheral systems, such as antiatherosclerosis, antineoplasms, antidiabetes; In recent years, people have also found curcumin’s therapeutic effects on some neurodegenerative diseases and affective disorders, such as alzheimer’s, parkinson’s, depression, epilepsy and anxiety. As a powerful antioxidative agent, curcumin can modulate the balance of redox and reduce the formation of responsive oxidative species(ROS), which results in the neuroprotective effect. In addition to these, the neuroprotective effect of curcumin is involved in regulating signal molecules, such as NF-κB Nrf2 p-MEK,p-ERK,c-fos,APP,BACE1.Curcumin can also affect the BDNF/TrkB-MAPK/PI-3K-CREB pathway to regulate the neuroplasticity, cell vitality and antiapoptosis. This review summarizes the effects and possible mechanism of curcumin on neurodegenerative diseases, cerebral ischemia, traumatic brain injury and affective disorders such as depression and anxiety.
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    Glucocorticoids and Hippocampal Structural Plasticity
    CHEN Lin,DU Li-jun,ZHAO Yu-nan
    2011, 1 (2):  58-64. 
    Abstract ( 4958 )   PDF (1023KB) ( 3384 )  
    Chronic high dose glucocorticoid exposure produces the major disruption to the hippocampal structural plasticity(such as plastic changes in spine and dendrite morphology, astrocyte as well as adult neurogenesis), which can be reversed by anti-glucocorticoid therapy,indicating that glucocorticoids play a crucial role in chronic stress-induced impairment of hippocampal structural plasticity. Thus, one way to avoid the variable effects of stress exposure on animal behavior is developed by using exogenous corticosterone administration as a means to enhance efficiency and stability of animal model. Interestingly, short-term or acute glucocorticoid exposure has the ability to enhance structural plasticity, suggesting that the regulation of glucocorticoids on hippocampal structural plasticity is bidirectional.
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