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1.
Neuroscience Bulletin ; (6): 271-276, 2007.
Article in English | WPRIM | ID: wpr-264714

ABSTRACT

<p><b>OBJECTIVE</b>To investigate lipopolysaccharide (LPS) induced acute cerebral inflammatory damage and the therapeutic effect of ginkgolide B (BN52021).</p><p><b>METHODS</b>Thirty Sprague-Dawley rats were randomly divided into 3 groups (n = 10 for each group): Control group, Model group and Treatment group (treated with BN52021). LPS were injected into the fourth ventricle of rat to make a neuroinflammatory murine model. Morris water maze was used to detect the learning and memory ability of rats; changes of synapse number and subcellular ultrastructures were observed under a transmission electron microscope; OX-42 positive microglia in the brain was detected by immunohistochemical method.</p><p><b>RESULTS</b>The average escape latency in the Treatment group were significantly shortened than that in the Model group; and the percentage of swimming distance traveled in platform quadrant accounting for total distance increased markedly. The rough endoplasmic reticulum and polyribosomes in the Treatment group were more than that in the Model group, but the number of synapses seemed to have no obvious change. The number of OX-42 positive microglia in the Treatment group decreased markedly than that in the Model group, and the grey density of OX-42-positive cells increased significantly.</p><p><b>CONCLUSION</b>LPS can induce inflammatory damages to the brain, but the damage could be antagonized by BN52021. Platelet activating factor receptor antagonist may offer an effective therapy for neurodegeneration diseases.</p>


Subject(s)
Animals , Rats , Behavior, Animal , Brain Diseases , Pathology , Fibrinolytic Agents , Therapeutic Uses , Ginkgolides , Therapeutic Uses , Hippocampus , Immunohistochemistry , Inflammation , Pathology , Lactones , Therapeutic Uses , Lipopolysaccharides , Toxicity , Maze Learning , Microglia , Metabolism , Microscopy, Electron, Transmission , Neurons , Platelet Activating Factor , Metabolism , Platelet Membrane Glycoproteins , Rats, Sprague-Dawley , Receptors, G-Protein-Coupled
2.
National Journal of Andrology ; (12): 1066-1071, 2006.
Article in Chinese | WPRIM | ID: wpr-289078

ABSTRACT

<p><b>OBJECTIVE</b>To observe the correlation between brain-derived neurotrophic factor (BDNF) expression in the nerve system of diabetes mellitus (DM) rats and diabetic erectile dysfunction (ED).</p><p><b>METHODS</b>DM rats were induced by injecting streptozotocin and erectile function test was done by injecting apomorphine (APO) at 1 month, 2 months, 3 months and 4 months. Then the brain, lumbosacral spinal cord, thoracic and lumbar sympathetic trunks, penis and prostate were taken from the diabetic and normal rats of the same age. The BDNF positive neurons and nerve fibers were shown by immunohistochemistry or fluorescence immunohistochemistry. The number and the grey density of BDNF positive cells and fibers were detected by image analysis.</p><p><b>RESULTS</b>Compared with the control group, the erection frequency of the DM rats decreased at 2 months (P <0. 05) , and significantly at 3 and 4 months (P > 0.01) , and the BDNF positive neurons and nerve fibers in the cerebral cortex, lumbosacral spinal cord, thoracic and lumbar sympathetic trunks, penis and prostate of 1-month DM rats were reduced (P <0. 05). As time went on, BDNF declined progressively.</p><p><b>CONCLUSION</b>BDNF decreases in the central and peripheral nerve system in the early stage of diabetes mellitus, wich is closely correlated with diabetic ED.</p>


Subject(s)
Animals , Male , Rats , Brain-Derived Neurotrophic Factor , Diabetes Mellitus, Experimental , Erectile Dysfunction , Nerve Tissue , Metabolism , Rats, Sprague-Dawley
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