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The relationships between the expressions of neurocyte adhesion molecule and growth associated protein-43 and the functional recovery following cerebral ischemia-reperfusion in rats

Zheng Qing-li

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Abstract

Objective To observe the effects of expressions of neurocyte adhesion molecule (NCAM) and growth associated protein-43 (GAP-43) in neurological function recovery following cerebral ischemia-reperfusion in rats. Methods The model of focal ischemia-reperfusion in SD rat was induced by intraluminal middle cerebral artery (MCA) occlusion with a nylon monofilament suture. In situ hybridization (ISH) was performed to examine the expression of NCAM mRNA and GAP-43 mRNA at 2,12 h and 1,2,3,7,14 d after reperfusion and in sham-operated controls. Results There was no functional deficit and little expression of NCAM mRNA and GAP-43 mRNA in brain cells in rats of the sham-operated group. In the experimental group, NCAM mRNA expression was observed after reperfusion for 2 h in cortex and striatum and peaked at 12 h and was still higher at 7 d. The neurological function improved at reperfusion of 3 d~14 d compared to reperfusion 2 h. In the ischemic cortex and striatum, GAP-43 mRNA expression demonstrated double-peak at 12 h and 2 d after reperfusion, then decreased gradually to the level of sham-operated group at 14 d. Conclusion The increasing NCAM expression might be an important factor of the neural reparation and GAP-43 might enhance the neurological functional recovery with ischemic brain injury in rat.

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What this paper is about

Objective To observe the effects of expressions of neurocyte adhesion molecule (NCAM) and growth associated protein-43 (GAP-43) in neurological function recovery following cerebral ischemia-reperfusion in rats. Methods The model of focal ischemia-reperfusion in SD rat was induced by intraluminal middle cerebral artery (MCA) occlusion with a nylon monofilament suture. In situ hybridization (ISH) was performed to examine the expression of NCAM mRNA and GAP-43 mRNA at 2,12 h and 1,2,3,7,14 d after reperfusion and in sham-operated controls. Results There was no functional deficit and little expression of NCAM mRNA and GAP-43 mRNA in brain cells in rats of the sham-operated group. In the experimental group, NCAM mRNA expression was observed after reperfusion for 2 h in cortex and striatum and peaked at 12 h and was still higher at 7 d. The neurological function improved at reperfusion of 3 d~14 d compared to reperfusion 2 h. In the ischemic cortex and striatum, GAP-43 mRNA expression demonstrated double-peak at 12 h and 2 d after reperfusion, then decreased gradually to the level of sham-operated group at 14 d. Conclusion The increasing NCAM expression might be an important factor of the neural reparation and GAP-43 might enhance the neurological functional recovery with ischemic brain injury in rat.

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Available abstract

Objective To observe the effects of expressions of neurocyte adhesion molecule (NCAM) and growth associated protein-43 (GAP-43) in neurological function recovery following cerebral ischemia-reperfusion in rats. Methods The model of focal ischemia-reperfusion in SD rat was induced by intraluminal middle cerebral artery (MCA) occlusion with a nylon monofilament suture. In situ hybridization (ISH) was performed to examine the expression of NCAM mRNA and GAP-43 mRNA at 2,12 h and 1,2,3,7,14 d after reperfusion and in sham-operated controls. Results There was no functional deficit and little expression of NCAM mRNA and GAP-43 mRNA in brain cells in rats of the sham-operated group. In the experimental group, NCAM mRNA expression was observed after reperfusion for 2 h in cortex and striatum and peaked at 12 h and was still higher at 7 d. The neurological function improved at reperfusion of 3 d~14 d compared to reperfusion 2 h. In the ischemic cortex and striatum, GAP-43 mRNA expression demonstrated double-peak at 12 h and 2 d after reperfusion, then decreased gradually to the level of sham-operated group at 14 d. Conclusion The increasing NCAM expression might be an important factor of the neural reparation and GAP-43 might enhance the neurological functional recovery with ischemic brain injury in rat.

Key concepts: Striatum, In situ hybridization, Ischemia, Messenger RNA, Neural cell adhesion molecule, Internal medicine, Reperfusion injury, Cerebral cortex

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