| 引用本文:潘晶晶，邹蕾，黄志远，孙香蕾.大麻素1型受体过表达对实验性自身免疫性脑脊髓炎小鼠神经干细胞的影响[J].世界中医药,2021,(19):. |
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| 大麻素1型受体过表达对实验性自身免疫性脑脊髓炎小鼠神经干细胞的影响 |
| Effect of CB1R Overexpression on Neural Stem Cells in EAE Mice |
| 投稿时间：2020-04-25 |
| DOI：10.3969/j.issn.1673-7202.2021.19.016 |
| 中文关键词: 大麻素1型受体 过表达 实验性自身免疫性脑脊髓炎 小鼠 脑组织室管膜下区 神经干细胞 5-溴-2'-脱氧尿苷 巢蛋白 |
| English Keywords:Cannabinoid 1 receptor Overexpression Experimental autoimmune encephalomyelitis Mice Subependymal area of brain tissue Neural stem cells 5-bromo-2'-deoxyuridine Nestin |
| 基金项目:辽宁省科技厅重点项目(2019010205) |
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| 中文摘要: |
| 目的:探讨大麻素1型受体(CB1R)过表达对实验性自身免疫性脑脊髓炎小鼠脑神经干细胞的影响。方法:建立EAE小鼠模型(n=50)并设置佐剂组(n=10)和对照组(n=10),建模成功的EAE小鼠注射CB1R过表达慢病毒液并记为CBlR过表达组(n=20),设置空载体组(n=10)和EAE模型组(n=20)。评价各组小鼠神经功能，观察对照组、EAE模型组和CBlR过表达组小鼠的脑组织病理学变化，检测脑组织CB1R、室管膜下区Brdu和Brdu+/Nestin+以及Sox-2 mRNA水平。结果：EAE模型组神经功能评分升高、CBlR蛋白降低(P<0.05),CBlR过表达组神经功能评分下降、CBlR蛋白升高(P<0.05)。EAE模型组脑组织出现炎症细胞浸润及髓鞘缺失等典型病理变化,CBlR过表达组的病理损伤显著改善。EAE模型组Brdu、Brdu+/Nestin+阳性细胞以及Sox-2mRNA水平均显著增加(均P<0.05),CBlR过表达组比较EAE模型组亦显著增加(P<0.05)。结论:过表达CBlR可能是通过加速小鼠脑神经干细胞的增殖从而促进脑组织损伤的修复,最终有效减轻了自身免疫性脑脊髓炎小鼠的症状。 |
| English Summary: |
| To investigate the effect of cannabinoid 1 receptor(CB1R) overexpression on cerebral nerve stem cells in mice with experimental autoimmune encephalomyelitis.Methods:EAE models(50 mice) were established,as well as an adjuvant group of 10 and a control group of 10 mice.In the models built successfully,EAE mice were injected with CB1R overexpression lentivirus and recorded as CBlR overexpression group(20 mice).Null vector group(10 mice) and the EAE model group(20 mice) were also set.Neurological functions of mice in each group were evaluated,pathological changes of brain tissue were observed,and levels of CB1R,Brdu and Brdu+/Nestin+ in subependymal area and SOX-2 mRNA of brain tissue were detected.Results:In the EAE model group,neurological function score increased and CBlR protein decreased(P<0.05),while neurological function score decreased and CBlR protein increased in the CBlR overexpression group(P<0.05).Typical pathological changes,such as inflammatory infiltration and myelin loss,occurred in the EAE model group.Pathological damage was significantly improved in the CBlR overexpression group.The levels of Brdu,Brdu+/Nestin+ positive cells and SOX-2 mRNA in the EAE model group were significantly increased(P<0.05),and so were the other two groups(P<0.05).Conclusion:Overexpression of CBlR may promote the repair of brain tissue damage by accelerating the proliferation of brain neural stem cells in mice,and effectively alleviate the symptoms of autoimmune encephalomyelitis in the end. |
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