摘要
目的:基于人类全基因表达谱芯片高通量测序技术,分析肾精亏虚证老年性痴呆发病机制与差异基因表达的相关性。方法:在辽宁中医药大学附属医院和上海中医药大学附属龙华医院门诊选择60岁以上16例肾精亏虚证AD患者,对照组为同龄健康状态老年人12例,男女各半。清晨取静脉血5 m L,加入百泰克生产血液总RNA快速提取试剂盒,-70℃保存。统一干冰冷冻寄送北京博奥生物有限公司,利用Affymetrix公司的Human Gene Expression Array基因表达谱芯片,分析两组基因差异表达。结果:肾精亏虚证AD患者特异性表达的探针有308个,对应247个基因(FC≥1.5,q-value≤5%),其中上调基因228个,下调基因19个。实时定量PCR验证了其中差异最大的9个基因的表达。结论:肾精亏虚证AD的发病机制之一与人类基因表达谱中9个差异表达基因调控有关。
Objective: To analyze the correlationship between the pathogenesis of Alzheimer's disease of kidney-essence deficiency( AD-KED) and gene expressionby high throughput gene sequencing. Methods: Sixteen AD-KED patients aged 60 ~ 75 years old,and 12 control with paired ages and genders were recruited from The First Affiliated Hospital of Liaoning University of Traditional Chinese Medicine and Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine. In the early morning,5 m L of blood was collected by vein,and lysed with RNA lysis buffer( made by Bio Teke),stored at-70 ℃. The samples were sent to Capital Bio Corporation of Beijing with dry ice and gene expression was analyzed using the Human Gene Expression Arraychip( Affymetrix's Prime ViewTM). Results: A total of 308 probes,representing 247 genes,were differentially expressed in AD-KED patients( FC≥1. 5,q-value≤5%). Within them,228 genes were up-regulated and 19 genes were down regulated. The expressions of 9 genes with the biggest difference were verified by real-time PCR. Conclusion: We confirmed the gene expression signature of patients with AD-KED. Conclusion: It is relatedgene regulation of 9 differentially expressed genes and one of the pathogenesis of AD withdeficiency of kidney-essence in human gene expression profiles.
作者
辛华
谢晚晴
蒋宁
孙丽
郑洪新
XIN Hua;XIE Wanqing;JIANG Ning;SUN Li;ZHENG Hongxin(Liaoning University of Traditional Chinese Medicine,Shenyang 110847,Liaoning,China)
出处
《中华中医药学刊》
CAS
北大核心
2018年第9期2078-2081,I0018,共5页
Chinese Archives of Traditional Chinese Medicine
基金
国家自然科学基金项目(81273612)
国家重点基础研究发展计划(973计划)项目(2010CB530401)
关键词
肾精亏虚
老年性痴呆
人类全基因表达谱
kidney essence deficiency
Alzheimer' s disease
human gene expression profiling