Effects of electroacupuncture on glial scar generation in SCI model rats

胶质纤维酸性蛋白 脊髓损伤 电针 H&E染色 免疫印迹 胶质瘢痕 豪华耐晒蓝 脊髓 波形蛋白 化学 海马体 免疫组织化学 内分泌学 中枢神经系统 医学 针灸科 内科学 病理 髓鞘 生物化学 替代医学 精神科 基因
作者
Yu Hu,Haobin Zhao,Suhua Shi,Yali Zhao,Xiaoming Gao,Jingwen Sun,Zhigang Li,Haijiang Yao
出处
期刊:Anatomical Record-advances in Integrative Anatomy and Evolutionary Biology [Wiley]
卷期号:306 (12): 3156-3168 被引量:1
标识
DOI:10.1002/ar.25132
摘要

Abstract Spinal cord injury (SCI) is a commonly occurring and severe form of central nervous system (CNS) injury. Previous studies have demonstrated that electroacupuncture (EA) therapy promotes recovery from SCI. In this study, we observed changes in the glial scars of rats with SCI to gain insight into how EA therapy positively influences locomotor function. The experimental rats were randomly divided into three groups: the sham group, the SCI group and the SCI + EA group. Rats in the SCI + EA group received a 28‐day treatment course using the Dazhui (GV14) acupoint and the Mingmen (GV4) acupoint for 20 min/day. The Basso–Beattie–Bresnahan (BBB) score was used to estimate the neural function of rats in all groups. We found that before sacrifice on Day 28, the BBB score was significantly improved in the SCI + EA group, which was higher than that observed in the SCI group. Hematoxylin–eosin staining revealed morphological improvements in spinal cord tissues of the rats in the EA + SCI group with reduced glial scars and cavities. Based on immunofluorescence staining, reactive astrocytes overpopulated both the SCI and SCI + EA groups following SCI. Moreover, improved generation of reactive astrocytes at lesions was observed in the SCI + EA group compared with the SCI group. After treatment, EA inhibited glial scar generation. EA effectively downregulated fibrillary acidic protein (GFAP) and vimentin protein and mRNA expression levels, according to the results from Western blot assays and reverse transcription–polymerase chain reaction (RT–PCR). We hypothesized that these findings described might represent the mechanism underlying EA inhibition of glial scar generation, morphological improvements in tissues and promotion of neural recovery from SCI in rats.
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