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圣草酚可改善脊髓损伤大鼠的功能恢复并减轻髓鞘损失。

Eriodictyol corrects functional recovery and myelin loss in SCI rats.

作者信息

Li Chenggang, Wang Chunfang

机构信息

Department of Orthopaedics, Second Hospital Shanxi Medical University, Taiyuan, Shanxi, 030001, China.

Laboratory Animal Center, Shanxi Medical University, Taiyuan, Shanxi, 030001, China.

出版信息

Transl Neurosci. 2020 Dec 31;11(1):439-446. doi: 10.1515/tnsci-2020-0128. eCollection 2020.

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.

摘要

背景

本研究调查了圣草酚(EDC)对脊髓损伤(SCI)大鼠的治疗潜力及其相关机制。

方法

采用重物坠落法在Sprague-Dawley大鼠中建立SCI模型。将SCI大鼠分为四组,即假手术组(仅行椎板切除术)、对照组(给予溶剂处理)、10mg/kg EDC处理组和20mg/kg EDC处理组。在诱导SCI后,通过蛛网膜下腔途径在腰4水平向SCI大鼠注射EDC或溶剂。进行旷场试验和倾斜平面试验以评估运动活性。对脊髓损伤部位进行组织病理学分析。通过蛋白质免疫印迹分析和免疫组织化学分析检测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)的表达。

结果

结果表明,EDC处理的大鼠运动活性显著改善,髓鞘损失也较低。大鼠还表现出Bcl-2和Bax的过表达。EDC治疗还增加了SCI后GCDNF和BDNF的水平。这些结果表明,EDC发挥了神经保护作用,并通过提高GCDNF和BDNF水平以及阻断凋亡相关蛋白来改善运动活性。

结论

本研究表明,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断。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175a/7917365/aa377c676b4a/j_tnsci-2020-0128-fig001.jpg

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