2007•Chinese Journal of NeuromedicineRequires access

Experimental study on inducement of ischemic brain injury to nestin expression of rats

Yang Wen-lian

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Abstract

Objective To probe into the effects of ischemic brain injury on proliferation and migration of endogenous neural stem cells(NSCs).Methods A total of 62 healthy male SD rats were randomly divided into the normal group(n=6),operation group,with 6 rats at each time point,42 rats in total(reperfusion at 1,3,5,7,10,15 or 20d after 10 min cerebral ischemia),and sham-operated control group(n=14,2 rats at each time point).The rat models with transient global cerebral ischemia were established by Pulsinelli-Brierley' s four-vessel occlusion;SABC immunohistochemistry was employed to show neuroepithelial stem cell protein(nestin)positive cells;the morphological changes ofnestin positive cells were observed under the optical microscope and their number was counted,for the semi-quantitative analysis of the change process in proliferation and migration of endogenous NSCs after ischemic brain injury.Results The expression ofnestin positive cells in the operation group increased 24h later after ischemia-reperfusion,achieved its climax between 7-10 d and was still obvious at 15d;there was evidence that nestin positive cells migrated from the SVZ to the cortex or hippocampus.Conclusion Ischemic brain injury may induce the proliferation of endogenous NSCs,which might exert effects for the recovery of brain injury.

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Objective To probe into the effects of ischemic brain injury on proliferation and migration of endogenous neural stem cells(NSCs).Methods A total of 62 healthy male SD rats were randomly divided into the normal group(n=6),operation group,with 6 rats at each time point,42 rats in total(reperfusion at 1,3,5,7,10,15 or 20d after 10 min cerebral ischemia),and sham-operated control group(n=14,2 rats at each time point).The rat models with transient global cerebral ischemia were established by Pulsinelli-Brierley' s four-vessel occlusion;SABC immunohistochemistry was employed to show neuroepithelial stem cell protein(nestin)positive cells;the morphological changes ofnestin positive cells were observed under the optical microscope and their number was counted,for the semi-quantitative analysis of the change process in proliferation and migration of endogenous NSCs after ischemic brain injury.Results The expression ofnestin positive cells in the operation group increased 24h later after ischemia-reperfusion,achieved its climax between 7-10 d and was still obvious at 15d;there was evidence that nestin positive cells migrated from the SVZ to the cortex or hippocampus.Conclusion Ischemic brain injury may induce the proliferation of endogenous NSCs,which might exert effects for the recovery of brain injury.

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Available abstract

Objective To probe into the effects of ischemic brain injury on proliferation and migration of endogenous neural stem cells(NSCs).Methods A total of 62 healthy male SD rats were randomly divided into the normal group(n=6),operation group,with 6 rats at each time point,42 rats in total(reperfusion at 1,3,5,7,10,15 or 20d after 10 min cerebral ischemia),and sham-operated control group(n=14,2 rats at each time point).The rat models with transient global cerebral ischemia were established by Pulsinelli-Brierley' s four-vessel occlusion;SABC immunohistochemistry was employed to show neuroepithelial stem cell protein(nestin)positive cells;the morphological changes ofnestin positive cells were observed under the optical microscope and their number was counted,for the semi-quantitative analysis of the change process in proliferation and migration of endogenous NSCs after ischemic brain injury.Results The expression ofnestin positive cells in the operation group increased 24h later after ischemia-reperfusion,achieved its climax between 7-10 d and was still obvious at 15d;there was evidence that nestin positive cells migrated from the SVZ to the cortex or hippocampus.Conclusion Ischemic brain injury may induce the proliferation of endogenous NSCs,which might exert effects for the recovery of brain injury.

Key concepts: Nestin, Endogeny, Neural stem cell, Ischemia, Neuroepithelial cell, Immunohistochemistry, Hippocampus, Medicine

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