大鼠侧脑室注射脂多糖选择性减少黑质神经生长因子的表达  被引量:2

Selective reduction of the expression of nerve growth factor in substantia nigra following introcerebroventricular injection of lipopolysaccharide in rats

在线阅读下载全文

作  者:周岩[1] 孙晓红[1] 刘玉军[1] 雷慧萌 徐群渊[1] 

机构地区:[1]首都医科大学神经生物学系北京市脑重大疾病研究院教育部神经变性病重点实验室,北京100069

出  处:《神经解剖学杂志》2015年第6期713-716,共4页Chinese Journal of Neuroanatomy

基  金:国家自然科学基金(31171051);北京市自然科学基金(7152015;5132007);北京市教委科技发展计划面上项目(KM201110025001)

摘  要:目的:探讨脑内慢性炎症对大鼠黑质部位神经生长因子(nerve growth factor,NGF)表达的影响以及是否具有选择性。方法:将脂多糖(lipopolysaccharide,LPS)单次注入SD大鼠侧脑室制成脑内慢性炎症帕金森病(Parkinson's disease,PD)模型在注射后的各个时间点分离出不同部位的脑组织并提取蛋白,通过Western Blot方法检测NGF在黑质和中缝背核的表达变化。结果:Western Blot检测显示在LPS注射后4周开始黑质中NGF的蛋白表达降低,并显著低于对照组,一直持续到24周;而中缝背核中实验组NGF的表达与对照组相比一直没有显著性变化。结论:脑内慢性炎症可以选择性减少黑质中NGF的表达,提示可能与脑内慢性炎症选择性损伤黑质多巴胺能神经元相关。Objective:To study the effect of chronic inflammation in rat brain on the expression of nerve growth factor(NGF) and the acting selectivity in the substantia nigra(SN).Methods:A single intracerebroventricular injection of lipopolysaccharide(LPS) was made to induce brain chronic inflammation model of Parkinson' s disease(PD).At certain time points,different parts of brain were dissected and the protein was extracted and the expression of NGF in the SN and the dorsal raphe nucleus was detected with Western Blot.Results:The expression of NGF in SN was reduced significantly from 4 weeks after LPS injection compared with the control group,decreasing continuously till 24 weeks.In contrast,the expression of NGF in the dorsal raphe nucleus had no significant change during the entire time course in the LPS group compared with the control group.Conclusion:Chronic inflammation in the brain can selectively reduce the expression of NGF in the SN.It might relate to the selective reduction of dopaminergic neurons in the SN caused by the chronic inflammation in the brain.

关 键 词:帕金森病 神经生长因子 黑质 炎症 大鼠 

分 类 号:R742.5[医药卫生—神经病学与精神病学]

 

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