Chenggang Li1, Chunfang Wang2. 1. Department of Orthopaedics, Second Hospital Shanxi Medical University, Taiyuan, Shanxi, 030001, China. 2. Laboratory Animal Center, Shanxi Medical University, Taiyuan, Shanxi, 030001, China.
Abstract
BACKGROUND: This study investigated the therapeutic potential of eriodictyol (EDC) in spinal cord injury (SCI) rats and also the mechanism involved. METHODS: The SCI model was created in Sprague-Dawley rats by the weight drop method. The SCI rats were divided into four groups, namely, Sham operated group (submitted for laminectomy only), control rats (vehicle treated), rats treated with 10 mg/kg EDC and rats treated with 20 mg/kg EDC. EDC or vehicle was injected in The SCI rats via subarachnoid route at the lumbar level 4 just after inducing SCI. The open field and inclined plane tests were done for assessing the locomotor activity. Histopathological analysis of the injured site of the spinal cord was done. Western blot analysis and immunohistochemical analysis were done for the expression of Bcl-2, Bax, glial cell line-derived neurotrophic factor (GCDNF) and brain-derived neurotrophic factor (BDNF). RESULTS: The outcomes suggested that EDC-treated rats showed significant improvement in the locomotor activity and also exhibited low myelin loss. The rats also showed overexpression of Bcl-2 and Bax. The treatment of EDC also increased the levels of GCDNF and BDNF after SCI. These outcomes suggested that EDC exerted the neuroprotective effect and also improved the locomotor activity by improving the levels of GCDNF and BDNF and blocking the apoptosis-related proteins. CONCLUSION: This study suggests that EDC could ameliorate the locomotor function, and the neuroprotective action may be attributed to modulation of GCDNF and BDNF and blockade of apoptosis-associated proteins.
BACKGROUND: This study investigated the therapeutic potential of eriodictyol (EDC) in spinal cord injury (SCI) rats and also the mechanism involved. METHODS: The SCI model was created in Sprague-Dawley rats by the weight drop method. The SCI rats were divided into four groups, namely, Sham operated group (submitted for laminectomy only), control rats (vehicle treated), rats treated with 10 mg/kg EDC and rats treated with 20 mg/kg EDC. EDC or vehicle was injected in The SCI rats via subarachnoid route at the lumbar level 4 just after inducing SCI. The open field and inclined plane tests were done for assessing the locomotor activity. Histopathological analysis of the injured site of the spinal cord was done. Western blot analysis and immunohistochemical analysis were done for the expression of Bcl-2, Bax, glial cell line-derived neurotrophic factor (GCDNF) and brain-derived neurotrophic factor (BDNF). RESULTS: The outcomes suggested that EDC-treated rats showed significant improvement in the locomotor activity and also exhibited low myelin loss. The rats also showed overexpression of Bcl-2 and Bax. The treatment of EDC also increased the levels of GCDNF and BDNF after SCI. These outcomes suggested that EDC exerted the neuroprotective effect and also improved the locomotor activity by improving the levels of GCDNF and BDNF and blocking the apoptosis-related proteins. CONCLUSION: This study suggests that EDC could ameliorate the locomotor function, and the neuroprotective action may be attributed to modulation of GCDNF and BDNF and blockade of apoptosis-associated proteins.
Authors: Emerson de Oliveira Ferreira; Mara Yone Soares Dias Fernandes; Neila Maria Rocha de Lima; Kelly Rose Tavares Neves; Marta Regina Santos do Carmo; Francisco Arnaldo Viana Lima; Analu Aragão Fonteles; Ana Paula Fontenele Menezes; Geanne Matos de Andrade Journal: Behav Brain Res Date: 2016-06-25 Impact factor: 3.332