中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (1): 137-142.doi: 10.4103/1673-5374.286973

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

电针干预高脂血症并大脑中动脉血栓形成大鼠海马胶质纤维酸性蛋白和神经生长因子的变化

  

  • 出版日期:2021-01-15 发布日期:2020-11-26
  • 基金资助:
    国家自然科学基金(81470200)

Effect of electroacupuncture on glial fibrillary acidic protein and nerve growth factor in the hippocampus of rats with hyperlipidemia and middle cerebral artery thrombus

Na-Ying Xue1, Dong-Yu Ge2, Rui-Juan Dong2, Hyung-Hwan Kim3, Xiu-Jun Ren1, *, Ya Tu1, *#br#   

  1. 1 School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, China;  2 School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China;  3 Neurovascular Research Laboratory, Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA
  • Online:2021-01-15 Published:2020-11-26
  • Contact: Xiu-Jun Ren, MD, PhD, rxiujun@163.com; Ya Tu, MD, PhD, tuyab@263.net.
  • Supported by:
    This study was funded by the National Natural Science Foundation of China, No. 81470200 (to XJR). 

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摘要：

研究表明，电针能够下调高血脂合并脑缺血大鼠的血脂水平，改善脑缺血。但有关电针是否能够在高血脂阶段降低血脂并促进脑卒中后神经修复的机制及实验结果尚不多。为此，实验以电针干预高血脂合并脑缺血模型大鼠观察海马区损伤后神经细胞的修复。高脂饲料喂养大鼠7周后建立高脂血症模型，第50天用50% FeCl3滤纸贴敷于左侧大脑中动脉20 min诱发高脂血合并大脑中动脉血栓大鼠模型设为模型组。大鼠造模前1周电针“丰隆穴”(ST40)，连续7 d，造模后电针“丰隆穴”(ST40)和“百会穴”(GV20)，连续14 d，设为电针1组；电针2组不进行电针预处理，其余干预方法同电针1组。（1）用血生化法检测血清血脂指标包括，总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白(LDL)和高密度脂蛋白(HDL)；（2）用免疫组织化学方法检测海马CA1区星形胶质细胞标记物胶质纤维酸性蛋白（GFAP）和神经生长因子（NGF）的表达；（3）结果发现，与模型组相比，电针1，2组大鼠的血脂水平和明显降低，海马CA1区胶质纤维酸性蛋白免疫反应明显减弱，神经生长因子免疫反应明显增强，电针1组的修复效果优于电针2组。说明在高脂血症合并大脑中动脉血栓状态下，采用电针干预能降低血脂水平，抑制海马CA1区胶质纤维酸性蛋白的分泌，并促进神经生长因子的分泌。

https://orcid.org/0000-0002-4912-0420 (Xiu-Jun Ren); 

https://orcid.org/0000-0002-6777-2588 (Ya Tu)

关键词:

电针, 高脂血症, 脑缺血, 星形胶质细胞, 胶质纤维酸性蛋白, 神经生长因子, 海马, CA1, 苏木精-伊红染色, 免疫组织化学

Abstract: Electroacupuncture (EA) has been shown to reduce blood lipid level and improve cerebral ischemia in rats with hyperlipemia complicated by cerebral ischemia. However, there are few studies on the results and mechanism of the effect of EA in reducing blood lipid level or promoting neural repair after stroke in hyperlipidemic subjects. In this study, EA was applied to a rat model of hyperlipidemia and middle cerebral artery thrombosis and the condition of neurons and astrocytes after hippocampal injury was assessed. Except for the normal group, rats in other groups were fed a high-fat diet throughout the whole experiment. Hyperlipidemia models were established in rats fed a high-fat diet for 6 weeks. Middle cerebral artery thrombus models were induced by pasting 50% FeCl3 filter paper on the left middle cerebral artery for 20 minutes on day 50 as the model group. EA1 group rats received EA at bilateral ST40 (Fenglong) for 7 days before the thrombosis. Rats in the EA1 and EA2 groups received EA at GV20 (Baihui) and bilateral ST40 for 14 days after model establishment. Neuronal health was assessed by hematoxylin-eosin staining in the brain. Hyperlipidemia was assessed by biochemical methods that measured total cholesterol, triglyceride, low-density lipoprotein and high-density lipoprotein in blood sera. Behavioral analysis was used to confirm the establishment of the model. Immunohistochemical methods were used to detect the expression of glial fibrillary acidic protein and nerve growth factor in the hippocampal CA1 region. The results demonstrated that, compared with the model group, blood lipid levels significantly decreased, glial fibrillary acidic protein immunoreactivity was significantly weakened and nerve growth factor immunoreactivity was significantly enhanced in the EA1 and EA2 groups. The repair effect was superior in the EA1 group than in the EA2 group. These findings confirm that EA can reduce blood lipid, inhibit glial fibrillary acidic protein expression and promote nerve growth factor expression in the hippocampal CA1 region after hyperlipidemia and middle cerebral artery thrombosis. All experimental procedures and protocols were approved by the Animal Use and Management Committee of Beijing University of Chinese Medicine, China (approval No. BUCM-3-2018022802-1002) on April 12, 2018. 

Key words: astrocytes, CA1, cerebral ischemia, electroacupuncture, glial fibrillary acidic protein, hematoxylin-eosin staining, hippocampus, hyperlipidemia, immunohistochemistry, nerve growth factor