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1.
Neuroscience Bulletin ; (6): 54-60, 2009.
Article in English | WPRIM | ID: wpr-264640

ABSTRACT

<p><b>OBJECTIVE</b>To prepare and identify a polyclonal antibody against rat myostatin and investigate myostatin expression in the rat atrophic gastrocnemius muscle after tibial nerve crush.</p><p><b>METHODS</b>The purified fusion protein was used as antigen to immunize rabbits for the preparation of polyclonal antibody. The polyclonal antibody of the protein was measured by enzyme linked immunosorbent assay (ELISA), western-blot and immunochemistry. Myostatin protein expression levels in normal and atrophic gastrocnemius muscle were detected by western-blot and immunochemistry assays.</p><p><b>RESULTS</b>The GST-myostatin had a purity of 96% and possessed high titer and specificity. The level of myostatin in gastrocnemius muscle significantly increased one week after tibial nerve crush, reached the peak on day 14, and then returned to normal level on day 28.</p><p><b>CONCLUSION</b>We have successfully made antiserum of rat myostatin and found that the expression level of myostatin protein in the gastrocnemius after tibial nerve crush-induced atrophy was time-dependent. This study provides an experimental basis to clarify the possible role of myostatin during skeletal muscle atrophy.</p>


Subject(s)
Animals , Female , Male , Rabbits , Rats , Analysis of Variance , Antibodies , Blood , Enzyme-Linked Immunosorbent Assay , Methods , Gene Expression Regulation , Physiology , Immune Sera , Immunization , Methods , Muscle, Skeletal , Metabolism , Myostatin , Allergy and Immunology , Rats, Sprague-Dawley , Recombinant Fusion Proteins , Allergy and Immunology , Tibial Neuropathy , Metabolism , Pathology , Time Factors
2.
Chinese Journal of Oncology ; (12): 663-667, 2008.
Article in Chinese | WPRIM | ID: wpr-255607

ABSTRACT

<p><b>OBJECTIVE</b>It is well known that glioma stem cells-progenitors (GSCP) proliferate indefinitely and hardly differentiate in vitro, however, the reasons remain unknown. The aim of this study was to explore the ultrastructural basis of GSCP.</p><p><b>METHODS</b>GSCP, kept by our laboratory, were collected, embedded, and cut into ultrathin sections and observed under the transmission electron microscope.</p><p><b>RESULTS</b>A single GSCP usually had relatively well developed mitochondria, Golgi apparatuses, ribosomes, and undeveloped rough endoplasmic reticulum, but seldom lysosomes and no typical autophagosomes were found, and the nuclear-cytoplasmic ratio was high. The nuclei frequently contained huge amounts of euchromatin and a small quantity of heterochromatin, and in most nuclei there were only one nucleolus, however, two or more nucleoli were also common. Typical apoptotic cells could hardly be found in tumor-spheres, and between neighboring cells in tumor-spheres there were incompletely developed desmosomes or intermediate junction.</p><p><b>CONCLUSION</b>The ultrastructural features of glioma stem cells-progenitors showed that BTSCP were very primitive and the lack of autophagy and the underdevelopment of some other cellular organelles are probably the reasons for the differential inhibition of GSCPs.</p>


Subject(s)
Humans , Brain Neoplasms , Cell Line, Tumor , Cell Membrane , Cell Nucleus , Chromatin , Cytoplasm , Glioma , Intercellular Junctions , Microscopy, Electron, Transmission , Mitochondria , Neoplastic Stem Cells
3.
Chinese Journal of Applied Physiology ; (6): 31-34, 2006.
Article in Chinese | WPRIM | ID: wpr-254613

ABSTRACT

<p><b>AIM</b>To observe protective effects of ginsenoside Rb3 on glutamate excitotoxic injury in cultured hippocampal neurons and involved mechanisms.</p><p><b>METHODS</b>On cultured rat hippocampal neurons treated with glutamate at toxic concentration, we made the following investigations: by using MTT assay, LDH leakage detection, tests of total NOS, iNOS and cNOS activity, and the protective effects of ginsenoside Rb3.</p><p><b>RESULTS</b>Ginsenoside Rb3 can enhance the hippocampal neuronal viability, decrease the LDH leakage, elevate the viability of cNOS, and in the same time weaken iNOS's viability.</p><p><b>CONCLUSION</b>Ginsenoside Rb3 has the significant protective effects on glutamate excitotoxic injury. The involved mechanism may include antagonizing the injury of neuron membrane, inhibiting the viability of iNOS, and increasing the activity of cNOS.</p>


Subject(s)
Animals , Rats , Animals, Newborn , Cells, Cultured , Ginsenosides , Pharmacology , Glutamic Acid , Hippocampus , Cell Biology , L-Lactate Dehydrogenase , Metabolism , Neurons , Metabolism , Neuroprotective Agents , Pharmacology , Nitric Oxide Synthase Type II , Metabolism , Rats, Sprague-Dawley
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