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[Expression of Nestin following focal cerebral ischemia-reperfusion in rats].

Xiao-Song Hu, De-Ming Zhou, Dong Zhou

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Abstract

OBJECTIVE: To study the expession of Nestin after focal ischemia-reperfusion in rats. METHODS: The model of acute reperfusion injury after cerebral ischemia in rat was made by middle cerebral artery occlusion. All animals were allowed 2 h ischemia and sacrificed after different durations of reperfusion (6 h, 12 h, 24 h, 72 h, 7 d, 14 d). The expression of Nestin was detected with an immunohistochemical approach. RESULTS: The number of Nestin- immunoreactive cells at 6 h after reperfusion in the ischemic side started to increase markedly and showed significant difference, compared with the Sham group (P < 0.05). The expression of Nestin and the number of Nestin positive cells with Brdu labeled peaked at 7 d after reperfusion and then were down-regulated at 14 d. CONCLUSION: The study implies cerebral ischemia could upregulate the expression of Nestin and induce the proliferation of nervous stem cells.

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OBJECTIVE: To study the expession of Nestin after focal ischemia-reperfusion in rats. METHODS: The model of acute reperfusion injury after cerebral ischemia in rat was made by middle cerebral artery occlusion. All animals were allowed 2 h ischemia and sacrificed after different durations of reperfusion (6 h, 12 h, 24 h, 72 h, 7 d, 14 d). The expression of Nestin was detected with an immunohistochemical approach. RESULTS: The number of Nestin- immunoreactive cells at 6 h after reperfusion in the ischemic side started to increase markedly and showed significant difference, compared with the Sham group (P < 0.05). The expression of Nestin and the number of Nestin positive cells with Brdu labeled peaked at 7 d after reperfusion and then were down-regulated at 14 d. CONCLUSION: The study implies cerebral ischemia could upregulate the expression of Nestin and induce the proliferation of nervous stem cells.

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Available abstract

OBJECTIVE: To study the expession of Nestin after focal ischemia-reperfusion in rats. METHODS: The model of acute reperfusion injury after cerebral ischemia in rat was made by middle cerebral artery occlusion. All animals were allowed 2 h ischemia and sacrificed after different durations of reperfusion (6 h, 12 h, 24 h, 72 h, 7 d, 14 d). The expression of Nestin was detected with an immunohistochemical approach. RESULTS: The number of Nestin- immunoreactive cells at 6 h after reperfusion in the ischemic side started to increase markedly and showed significant difference, compared with the Sham group (P < 0.05). The expression of Nestin and the number of Nestin positive cells with Brdu labeled peaked at 7 d after reperfusion and then were down-regulated at 14 d. CONCLUSION: The study implies cerebral ischemia could upregulate the expression of Nestin and induce the proliferation of nervous stem cells.

Key concepts: Nestin, Ischemia, Immunohistochemistry, Middle cerebral artery, Medicine, Downregulation and upregulation, Reperfusion injury, Pathology

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[Expression of Nestin following focal cerebral ischemia-reperfusion in rats]. — Research Paper | ScholarLens