加味温胆汤含药血清对DISC1基因突变小鼠神经元突起的影响  

The effects of Jiawei Wendan decoction medicated serum on neurite of DISC1 mutated mice

在线阅读下载全文

作  者:孙玉浩 温小雨 李卓娴 徐丽静 夏猛 Sun Yuhao;Wen Xiaoyu;Li Zhuoxian;Xu Lijing;Xia Meng(Basic Medicine,Guangxi University of Chinese Medicine,Nanning 530200,China)

机构地区:[1]广西中医药大学基础医学院,南宁530200

出  处:《神经解剖学杂志》2021年第6期670-676,共7页Chinese Journal of Neuroanatomy

基  金:国家自然科学基金(81302930;81860805);广西中医药大学歧黄高层次人才团队培育项目(2008001);广西中医药大学2017年青年创新研究团队项目(2017QTO01);广西中医药大学―流学科建设项目重点课题(2018XKO10);广西中医药基础研究重点实验室自主研究课题(KJT1904201);广西中医药大学研究生科研创新项目(YCSW2021234)。

摘  要:目的:探讨加味温胆汤对DISC1Esv 1转基因小鼠原代神经元发育的干预作用.方法:采用Tet-off系统调节DISC1Esv 1基因在小鼠原代神经元中的表达,在加味温胆汤含药血清干预下,利用荧光免疫、激光共聚焦显微镜技术观察原代神经元树突长度及兴奋性神经突触的影响情况.结果:在DISC1 Esv 1基因过表达的原代神经元中,其树突长度、兴奋性神经突触均有减少,经过加味温胆汤含药血清治疗后可显著改善原代神经元的树突长度、兴奋性神经突触的数量.结论:加味温胆汤对DISC1 Esv 1基因导致的神经元发育异常具有修复作用,加味温胆汤可能是通过修复受损的神经元发挥治疗作用.Objective: To investigate the effect of Jiawei Wendan Decoction on the development of primary neurons in DISC1 Esv 1 transgenic mice. Methods: The expression of DISC1 Esv 1 gene in primary neurons was regulated by Tet-off system. Under the intervention of serum containing Jiawei Wendan Decoction, the effects of dendrites length and excitatory synapse of primary neurons were observed by fluorescence immunoassay and laser confocal microscopy. Results: The length of dendrites and the number of excitatory synapses were decreased in the primary neurons overexpressed with DISC1 Esv 1 gene. After treatment with the serum containing Jiawei Wendan Decoction, the length of dendrites and the number of excitatory synapses were significantly improved. Conclusion: Jiawei Wendan Decoction can repair the abnormal development of neurons caused by DISC1 Esv 1 gene, and Jiawei Wendan decoction may play a therapeutic role by repairing the damaged neurons.

关 键 词:加味温胆汤 Tet-off系统 精神分裂症断裂基因1Esv1亚型转基因小鼠 原代神经元 

分 类 号:R285.5[医药卫生—中药学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象