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.

中文翻译：

---

Eriodictyol可纠正SCI大鼠的功能恢复和髓磷脂丢失。

背景技术这项研究探讨了香蒲醇（EDC）在脊髓损伤（SCI）大鼠中的治疗潜力以及所涉及的机制。方法采用失重法建立Sprague-Dawley大鼠SCI模型。将SCI大鼠分为四组，即假手术组（仅接受椎板切除术），对照组（经车辆处理），用10 mg / kg EDC治疗的大鼠和用20 mg / kg EDC治疗的大鼠。诱导SCI后，通过蛛网膜下腔途径在腰椎4级向SCI大鼠注射EDC或赋形剂。进行了开阔视野和倾斜平面测试，以评估运动能力。对脊髓损伤部位进行了组织病理学分析。进行了蛋白质印迹分析和免疫组化分析以检测Bcl-2，Bax，胶质细胞源性神经营养因子（GCDNF）和脑源性神经营养因子（BDNF）。结果结果表明，经EDC治疗的大鼠运动能力明显改善，髓磷脂损失也较低。大鼠还显示出Bcl-2和Bax的过度表达。SDC后EDC的治疗也增加了GCDNF和BDNF的水平。这些结果表明，EDC可以通过改善GCDNF和BDNF的水平并阻断凋亡相关蛋白来发挥神经保护作用，并改善运动能力。结论本研究提示EDC可改善运动功能，其神经保护作用可能归因于对GCDNF和BDNF的调节以及对凋亡相关蛋白的阻滞。结果结果表明，经EDC治疗的大鼠运动能力明显改善，髓磷脂损失也较低。大鼠还显示出Bcl-2和Bax的过度表达。SDC后EDC的治疗也增加了GCDNF和BDNF的水平。这些结果表明，EDC可以通过改善GCDNF和BDNF的水平并阻断凋亡相关蛋白来发挥神经保护作用，并改善运动能力。结论本研究提示EDC可改善运动功能，其神经保护作用可能归因于对GCDNF和BDNF的调节以及对凋亡相关蛋白的阻滞。结果结果表明，经EDC治疗的大鼠运动能力明显改善，髓磷脂损失也较低。大鼠还显示出Bcl-2和Bax的过度表达。SDC后EDC的治疗也增加了GCDNF和BDNF的水平。这些结果表明，EDC可以通过改善GCDNF和BDNF的水平并阻断凋亡相关蛋白来发挥神经保护作用，并改善运动能力。结论本研究提示EDC可改善运动功能，其神经保护作用可能归因于对GCDNF和BDNF的调节以及对凋亡相关蛋白的阻滞。SDC后EDC的治疗也增加了GCDNF和BDNF的水平。这些结果表明，EDC可以通过改善GCDNF和BDNF的水平并阻断凋亡相关蛋白来发挥神经保护作用，并改善运动能力。结论本研究提示EDC可改善运动功能，其神经保护作用可能归因于对GCDNF和BDNF的调节以及对凋亡相关蛋白的阻滞。SDC后EDC的治疗也增加了GCDNF和BDNF的水平。这些结果表明，EDC可以通过改善GCDNF和BDNF的水平并阻断凋亡相关蛋白来发挥神经保护作用，并改善运动能力。结论本研究提示EDC可改善运动功能，其神经保护作用可能归因于对GCDNF和BDNF的调节以及对凋亡相关蛋白的阻滞。