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1.
Chinese Medical Journal ; (24): 275-280, 2005.
Article in English | WPRIM | ID: wpr-250943

ABSTRACT

<p><b>BACKGROUND</b>There are no reports on exnografting cultured human fetal neocortical cells in this infracted cavities of adult rat brains. This study was undertaken to observe whether cultured human cortical neurons and astrocytes can survive and grow in the infarcted cavities of adult rat brains and whether they interconnect with host brains.</p><p><b>METHODS</b>The right middle cerebral artery was ligated distal to the striatal branches in 16 adult stroke-prone renovascular hypertensive rats. One week later, cultured cells from human embryonic cerebral cortexes were stereotaxically transferred to the infarcted cavity of 11 rats. The other 5 rats receiving sham transplants served as controls. For immunosuppression, all transplanted rats received intraperitoneal injection of cyclosporine A daily starting on the day of grafting. Immunohistochemistry for glial fibrillary acidic protein (GFAP), synaptophysin, neurofilament, and microtubule associated protein-2 (MAP-2) was performed on brain sections perfused in situ 8 weeks after transplantation.</p><p><b>RESULTS</b>Grafts in the infarcted cavities of 6 of 10 surviving rats consisted of bands of neurons with an immature appearance, bundles of fibers, and GFAP-immunopositive astrocytes, which were unevenly distributed. The grafts were rich in synaptophysin, neurofilament, and MAP2-positive neurons with long processes. The graft/host border was diffuse with dendrites apparently bridging over to the host brain, into which neurofilament immunopositive fibers protruded.</p><p><b>CONCLUSION</b>Cultured human fetal brain cells can survive and grow in the infarcted cavities of immunodepressed rats and integrate with the host brain.</p>


Subject(s)
Animals , Humans , Rats , Astrocytes , Transplantation , Brain , Pathology , Cell Proliferation , Cell Survival , Cells, Cultured , Cerebral Infarction , Metabolism , Pathology , Therapeutics , Fetal Tissue Transplantation , Glial Fibrillary Acidic Protein , Microtubule-Associated Proteins , Neocortex , Cell Biology , Neurons , Transplantation , Synaptophysin
2.
Chinese Journal of Integrated Traditional and Western Medicine ; (12): 531-533, 2002.
Article in Chinese | WPRIM | ID: wpr-304206

ABSTRACT

<p><b>OBJECTIVE</b>To explore the mechanism of rehabilitation after middle cerebral artery occlusion (MCAO).</p><p><b>METHODS</b>MCAO model was reproduced with two-kidney, two clip renovascular hypertensive rats stroke-prone (RHRSP), which were divided into two groups, the treated group (treated with electric stimulus) and the control group (untreated model) randomly. The rehabilitation of rats was evaluated by balance beam walking test. The ultrastructural changes of neurons and astrocytes, expressions of glial fibrillary acidic protein (GFAP)-positive cells, neurofilament (NF) protein, and cerebral capillary dilatation M-associated protein-2 (MAP2), as well as the neurons apoptosis and the number of dilatation of cerebral capillary in the margin of infarcted area were observed by the end of 1st, 3rd, 6th and 9th week after modeling.</p><p><b>RESULTS</b>The motor function of paralysed limbs recovered better in the treated group than that in the control group by the end of 3-9th week after MCAO, the expression of GFAP-positive cells in astrocytes and NF, MAP2 in neurons as well as the number of cerebral capillary dilatation at the margin of infarcted area were higher than those in the control group (P < 0.05).</p><p><b>CONCLUSION</b>Electric stimulation treatment could improve the recovery of motor function of paralyzed limbs. It might be due to the effect of electric stimulus in increasing astrocytes proliferation, reinforcing activity of neurons and evoking the dilatation of cerebral capillary.</p>


Subject(s)
Animals , Male , Rats , Apoptosis , Astrocytes , Electric Stimulation Therapy , Glial Fibrillary Acidic Protein , Metabolism , Infarction, Middle Cerebral Artery , Pathology , Rehabilitation , Neurons , Random Allocation , Rats, Sprague-Dawley
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