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Neural stem cell activation and proliferation in situ after intracerebral hemorrhage:an experimental study in adult rats

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Author:
No author available
Journal Title:
CHINESE JOURNAL OF NEUROMEDICINE
Issue:
10
DOI:
10.3760/cma.j.issn.1671-8925.2008.10.007
Key Word:
脑出血;神经干细胞;神经功能缺损;Intracerebral hemorrhage;Neural stem cells;Neurological function defect

Abstract: Objective To observe neural stem cell activation and proliferation in situ afterintracerebal hemorrhage (ICH) and its effect on the neurological function of the injured adult rats.Methods Seventy-two adult rats were randomized into ICH and sham operation groups (n=36). In theICH group, type Ⅳ collagenase was injected into the internal capsule through a microinfusion pump toinduce intracerebral hemorrhage, and the rats in the sham operation group received only phosphate buffersolution injection. The neurological functions of the rats were observed by rotarod motor test on days 1, 7,14, 21, 28, and 35 after the injection. One day before sacrifice, the rots were subjected to intraperitonealBrdU injection to label the regenerated cells, and immunohistochemistry was used to detect theexpressions of nestin and BrdU in the brain tissue. Results No nestin- or BrdU-positive cells werefound in the brain of the rats in the sham operation group. In rats with ICH, nestin- and BrdU-positivecells were found predominantly in the basal ganglion around the hematoma, in the ependyma and near thesubventricular zone (SVZ) in the brain; the number of the positive cells increased significantly 7 daysafter ICH, peaked on day 14 and then significantly reduced on day 28. The rats exhibited no obviousimprovement of the impaired motor function over the period from day 1 to 35 after ICH. Activation andproliferation of the neural stem cells was not obviously related to the recovery of the neurologicalfunctions. Conclusion Endogeneous neural stem cells in the brain are activated in rats after ICH, butthese stem cells possess rather limited capacity of proliferation and can not sufficiently compensate forICH-induced neurological function impairment.

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