[Effect of ventricle injection of Nogo-A antibody on neuronal regeneration following hypoxic-ischemic brain damage in the neonatal rat].
Xiao-Guang Zhou, Renhong Liu, Aihua Xiong
Abstract
Xiao-Guang Zhou, Renhong Liu, Aihua Xiong
Abstract
OBJECTIVE: Nogo-A antibody IN-1 can neutralize Nogo-A, a neurite growth inhibitory protein, promoting axonal regeneration following lesions of the central nervous system (CNS) in adult rats. This study aimed to examine the effect of ventricle injection of Nogo-A antibody on neuronal regeneration in neonatal rats following hypoxic-ischemic brain damage (HIBD). METHODS: A model of neonatal HIBD was prepared by the ligation of the left common carotid artery, followed by 8% hypoxia exposure. Forty HIBD rats were randomly given a ventricle injection of 10 microL Nogo-A antibody IN-1 (IN-1 group) or 10 microL artificial cerebrospinal fluid (artificial CSF group) (n=20 each). Another 20 neonatal rats were sham-operated, without hypoxia-ischemia, and were used as the controls. The levels of Nogo-A and GAP-43 protein in the brain were measured by immunohistochemistry. RESULTS: The number of immunohistory positive cells of Nogo-A in the brain in the IN-1 group (28.61+/-1.70) was obviously less than that in the artificial CSF (39.52 +/-1.40) and the sham-operated groups (32.78 +/- 1.87) (both P < 0.01). There were significant differences in the Nogo-A protein expression between the artificial CSF and the sham-operated groups (P < 0.01). The GAP-43 protein expression in the IN-1 group (31.14 +/- 1.88) was noticeably higher than that in the artificial CSF group (27.73 +/- 1.43 ) (P < 0.01). Both the IN-1 and the artificial CSF groups showed lower GAP-43 protein levels than the sham-operated groups (33.64 +/- 1.24) (both P < 0.01). CONCLUSIONS: Nogo-A antibody can reduce the expression of Nogo-A protein in the brain and thus promote neuronal regeneration in neonatal rats following HIBD. An increased GAP-43 protein expression in the brain after Nogo-A antibody administration shows an enhanced neuronal regeneration in the neonatal rats following HIBD.
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OBJECTIVE: Nogo-A antibody IN-1 can neutralize Nogo-A, a neurite growth inhibitory protein, promoting axonal regeneration following lesions of the central nervous system (CNS) in adult rats. This study aimed to examine the effect of ventricle injection of Nogo-A antibody on neuronal regeneration in neonatal rats following hypoxic-ischemic brain damage (HIBD). METHODS: A model of neonatal HIBD was prepared by the ligation of the left common carotid artery, followed by 8% hypoxia exposure. Forty HIBD rats were randomly given a ventricle injection of 10 microL Nogo-A antibody IN-1 (IN-1 group) or 10 microL artificial cerebrospinal fluid (artificial CSF group) (n=20 each). Another 20 neonatal rats were sham-operated, without hypoxia-ischemia, and were used as the controls. The levels of Nogo-A and GAP-43 protein in the brain were measured by immunohistochemistry. RESULTS: The number of immunohistory positive cells of Nogo-A in the brain in the IN-1 group (28.61+/-1.70) was obviously less than that in the artificial CSF (39.52 +/-1.40) and the sham-operated groups (32.78 +/- 1.87) (both P < 0.01). There were significant differences in the Nogo-A protein expression between the artificial CSF and the sham-operated groups (P < 0.01). The GAP-43 protein expression in the IN-1 group (31.14 +/- 1.88) was noticeably higher than that in the artificial CSF group (27.73 +/- 1.43 ) (P < 0.01). Both the IN-1 and the artificial CSF groups showed lower GAP-43 protein levels than the sham-operated groups (33.64 +/- 1.24) (both P < 0.01). CONCLUSIONS: Nogo-A antibody can reduce the expression of Nogo-A protein in the brain and thus promote neuronal regeneration in neonatal rats following HIBD. An increased GAP-43 protein expression in the brain after Nogo-A antibody administration shows an enhanced neuronal regeneration in the neonatal rats following HIBD.
Key concepts: Ventricle, Brain damage, Medicine, Cerebrospinal fluid, Hypoxia (environmental), Gap-43 protein, Ligation, Antibody