Naringin Treatment Improves Functional Recovery by Increasing BDNF and VEGF Expression, Inhibiting Neuronal Apoptosis After Spinal Cord Injury

The aim of this study was to determine the therapeutic efficacy of starting naringin treatment 1 day after spinal cord injury (SCI) in rat and to investigate the underlying mechanism. SCI was induced using the modified weight-drop method in Sprague–Dawley rats. The SCI animals were randomly divided...

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Veröffentlicht in:Neurochemical research 2012-08, Vol.37 (8), p.1615-1623
Hauptverfasser: Rong, Wei, Wang, Jun, Liu, Xiaoguang, Jiang, Liang, Wei, Feng, Hu, Xing, Han, Xiaoguang, Liu, Zhongjun
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container_issue 8
container_start_page 1615
container_title Neurochemical research
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creator Rong, Wei
Wang, Jun
Liu, Xiaoguang
Jiang, Liang
Wei, Feng
Hu, Xing
Han, Xiaoguang
Liu, Zhongjun
description The aim of this study was to determine the therapeutic efficacy of starting naringin treatment 1 day after spinal cord injury (SCI) in rat and to investigate the underlying mechanism. SCI was induced using the modified weight-drop method in Sprague–Dawley rats. The SCI animals were randomly divided into three groups: vehicle-treated group; 20 mg/kg naringin-treated group; 40 mg/kg naringin-treated group, and additionally with sham group (laminectomy only). Locomotors functional recovery was assessed during the 6 weeks post operation period by performing open-field locomotors tests and inclined-plane tests. At the end of the study, the segments of spinal cord encompassing the injury site were removed for histopathological analysis. Immunohistochemistry was performed to observe the expression of the brain-derived neurotrophic factor (BDNF). The expression of vascular endothelial growth factor (VEGF), B-cell CLL/lymphoma-2 (Bcl-2), BCL-2-associated X protein (Bax) and caspase-3 were detected by Western blot analysis. The apoptotic neural cells were assessed using the TUNEL method. The results showed that the naringin-treated animals had significantly better locomotor function recovery, less myelin loss, and higher expression of BDNF and VEGF. In addition, naringin treatment significantly increased in Bcl-2:Bax ratio, reduced the enzyme activity of caspase-3 and decreased the number of apoptotic cells after SCI. These findings suggest that naringin treatment starting 1 day after SCI can significantly improve locomotor recovery, and this neuroprotective effect may be related to the upregulation of BDNF and VEGF and the inhibition of neural apoptosis. Therefore, naringin may be useful as a promising therapeutic agent for SCI.
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SCI was induced using the modified weight-drop method in Sprague–Dawley rats. The SCI animals were randomly divided into three groups: vehicle-treated group; 20 mg/kg naringin-treated group; 40 mg/kg naringin-treated group, and additionally with sham group (laminectomy only). Locomotors functional recovery was assessed during the 6 weeks post operation period by performing open-field locomotors tests and inclined-plane tests. At the end of the study, the segments of spinal cord encompassing the injury site were removed for histopathological analysis. Immunohistochemistry was performed to observe the expression of the brain-derived neurotrophic factor (BDNF). The expression of vascular endothelial growth factor (VEGF), B-cell CLL/lymphoma-2 (Bcl-2), BCL-2-associated X protein (Bax) and caspase-3 were detected by Western blot analysis. The apoptotic neural cells were assessed using the TUNEL method. The results showed that the naringin-treated animals had significantly better locomotor function recovery, less myelin loss, and higher expression of BDNF and VEGF. In addition, naringin treatment significantly increased in Bcl-2:Bax ratio, reduced the enzyme activity of caspase-3 and decreased the number of apoptotic cells after SCI. These findings suggest that naringin treatment starting 1 day after SCI can significantly improve locomotor recovery, and this neuroprotective effect may be related to the upregulation of BDNF and VEGF and the inhibition of neural apoptosis. 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SCI was induced using the modified weight-drop method in Sprague–Dawley rats. The SCI animals were randomly divided into three groups: vehicle-treated group; 20 mg/kg naringin-treated group; 40 mg/kg naringin-treated group, and additionally with sham group (laminectomy only). Locomotors functional recovery was assessed during the 6 weeks post operation period by performing open-field locomotors tests and inclined-plane tests. At the end of the study, the segments of spinal cord encompassing the injury site were removed for histopathological analysis. Immunohistochemistry was performed to observe the expression of the brain-derived neurotrophic factor (BDNF). The expression of vascular endothelial growth factor (VEGF), B-cell CLL/lymphoma-2 (Bcl-2), BCL-2-associated X protein (Bax) and caspase-3 were detected by Western blot analysis. The apoptotic neural cells were assessed using the TUNEL method. The results showed that the naringin-treated animals had significantly better locomotor function recovery, less myelin loss, and higher expression of BDNF and VEGF. In addition, naringin treatment significantly increased in Bcl-2:Bax ratio, reduced the enzyme activity of caspase-3 and decreased the number of apoptotic cells after SCI. These findings suggest that naringin treatment starting 1 day after SCI can significantly improve locomotor recovery, and this neuroprotective effect may be related to the upregulation of BDNF and VEGF and the inhibition of neural apoptosis. 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SCI was induced using the modified weight-drop method in Sprague–Dawley rats. The SCI animals were randomly divided into three groups: vehicle-treated group; 20 mg/kg naringin-treated group; 40 mg/kg naringin-treated group, and additionally with sham group (laminectomy only). Locomotors functional recovery was assessed during the 6 weeks post operation period by performing open-field locomotors tests and inclined-plane tests. At the end of the study, the segments of spinal cord encompassing the injury site were removed for histopathological analysis. Immunohistochemistry was performed to observe the expression of the brain-derived neurotrophic factor (BDNF). The expression of vascular endothelial growth factor (VEGF), B-cell CLL/lymphoma-2 (Bcl-2), BCL-2-associated X protein (Bax) and caspase-3 were detected by Western blot analysis. The apoptotic neural cells were assessed using the TUNEL method. The results showed that the naringin-treated animals had significantly better locomotor function recovery, less myelin loss, and higher expression of BDNF and VEGF. In addition, naringin treatment significantly increased in Bcl-2:Bax ratio, reduced the enzyme activity of caspase-3 and decreased the number of apoptotic cells after SCI. These findings suggest that naringin treatment starting 1 day after SCI can significantly improve locomotor recovery, and this neuroprotective effect may be related to the upregulation of BDNF and VEGF and the inhibition of neural apoptosis. Therefore, naringin may be useful as a promising therapeutic agent for SCI.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>22453521</pmid><doi>10.1007/s11064-012-0756-7</doi><tpages>9</tpages></addata></record>
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subjects Animals
Apoptosis
Bax protein
Bcl-2 protein
bcl-2-Associated X Protein
Biochemistry
Biomedical and Life Sciences
Biomedicine
Brain-derived neurotrophic factor
Brain-Derived Neurotrophic Factor - biosynthesis
Caspase Inhibitors
Caspase-3
Cell Biology
Chronic lymphatic leukemia
Enzymes
Female
Flavanones - administration & dosage
Flavanones - therapeutic use
Immunohistochemistry
Lymphocytes B
Motor Activity - drug effects
Myelin
Myelin Sheath - drug effects
Neurochemistry
Neurology
Neuroprotection
Neurosciences
Original Paper
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rats
Rats, Sprague-Dawley
Recovery of function
Recovery of Function - drug effects
Spinal Cord Injuries - drug therapy
Spinal Cord Injuries - physiopathology
Spinal cord injury
Vascular endothelial growth factor
Vascular Endothelial Growth Factor A - biosynthesis
Western blotting
X protein
title Naringin Treatment Improves Functional Recovery by Increasing BDNF and VEGF Expression, Inhibiting Neuronal Apoptosis After Spinal Cord Injury
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