| 郑碧娥,何进娣,缪晓影,苏玲玲,范建中,尹瑞雪.磁疗对双环己酮草酰二腙诱导脱髓鞘小鼠的神经保护作用[J].中国康复医学杂志,2020,(10):1181~1186 |
| 磁疗对双环己酮草酰二腙诱导脱髓鞘小鼠的神经保护作用 点此下载全文 |
| 郑碧娥 何进娣 缪晓影 苏玲玲 范建中 尹瑞雪 |
| 南方医科大学南方医院康复医学科，广东省广州市，510515 |
| 基金项目：广东省自然科学基金项目(2016A030313523) |
| DOI：10.3969/j.issn.1001-1242.2020.10.005 |
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| 摘要： |
| 摘要
目的：探讨磁疗对双环己酮草酰二腙（cuprizone，CPZ）诱导脱髓鞘小鼠的神经保护作用及潜在机制。
方法：将30只雄性C57BL/6小鼠随机分为正常组、CPZ组和磁疗组，每组10只。CPZ组和磁疗组喂养0.3% CPZ的混合饲料建立脱髓鞘模型，磁疗组小鼠在实验第2周开始接受磁场（50Hz，10mT，每天20min，每周6d，共4周）的干预。每周称重记录各组小鼠的体质量。实验第5周末，利用转棒试验评估小鼠的运动功能；处死小鼠，免疫组化染色检测海马区的髓鞘碱性蛋白（MBP）和酶联免疫吸附（ELISA）测定脑源性神经营养因子（BDNF）的表达。
结果：第5周末，CPZ组和磁疗组小鼠体质量均明显低于正常组（P＜0.01）；磁疗组小鼠体质量有增长趋势，但与CPZ组相比差异不显著（P＞0.05）。与正常组相比，CPZ组小鼠运动功能明显下降(P<0.05)，海马区发生明显脱髓鞘改变、表现为MBP含量显著减少（P＜0.001），BDNF表达下降（P＜0.01）。与CPZ组相比，磁疗组小鼠的运动障碍得到改善(P<0.05)，髓鞘脱失有好转，MBP含量和BDNF表达均明显增多(P＜0.05,P<0.01)。
结论：磁疗具有改善CPZ模型小鼠的神经功能缺损和促进病灶内髓鞘修复的作用，其机制可能与上调脑内BDNF的表达有关。 |
| 关键词：磁疗法 脱髓鞘疾病 双环己酮草酰二腙 神经保护 脑源性神经营养因子 |
| Neuroprotective effects of magnetotherapy on cuprizone-induced demyelination in mice Download Fulltext |
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| Nanfang Hospital, Southern Medical University, Guangzhou, 510515 |
| Fund Project: |
| Abstract: |
| Abstract
Objective: To investigate neuroprotective effects of magnetotherapy on cuprizone (CPZ)-induced demyelination in mice and the underlying mechanism.
Method: Totally 30 male C57BL/6J mice were randomly divided into normal group，CPZ group and magnetotherapy group, 10 mice per group. Mice in CPZ and magnetotherapy group were fed a 0.3% CPZ to establish a demyelinating model. Beginning the second week of demyelinating feeding, mice of magnetotherapy group were treated by the magnetotherapy (10mT, 50Hz for 20 min/day，6 days/week，4 weeks in total). Body weight of each group mice was weekly weighed. Fifth week later, rotarod test was used to evaluate the motor function of mice. After mice sacrificed, myelin basic protein (MBP) and brain-derived neurotrophic factor (BDNF) in the hippocampus were assessed by immunohistochemical staining and enzyme-linked immunosorbent assay (ELISA) respectively.
Result: At the end of the fifth week, body weight in CPZ and magnetotherapy groups was both significantly less than it in normal group (P<0.01). In comparison to CPZ group, the body weight in magnetotherapy group had an increasing trend, but no significant difference (P>0.05). Compared with the normal group, the motor function of mice in CPZ group significantly decreased (P<0.05), the hippocampus had a significant demyelinating and the content of MBP markedly decreased (P<0.001), and the expression of BDNF significantly decreased (P＜0.01). Compared with the CPZ group, the motor function of mice in magnetotherapy group significantly ameliorated (P<0.05), changes of the demyelination improved, the MBP and BDNF significantly increased (P＜0.05 and P<0.01, respectively).
Conclusion: Magnetotherapy can ameliorate the neurobehavioral deficits and promote the recovery of demyelinating myelin in CPZ-induced mice，and the mechanism may be related to up-regulate the expression of BDNF in the brain. |
| Keywords:magnetotherapy demyelinating disease cuprizone neuroprotective brain-derived neurotrophic factor |
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