脾气虚证免疫相关基因组学机制初探

目的 采用CDNA芯片技术，探讨脾气虚证免疫功能的异常变化，并揭示其发生的基因组学机制。方法 分别提取脾气虚证慢性胃炎与溃疡性结肠炎患者(6例)以及健康人(3名)外周血白细胞总RNA，mRNA微量扩增，制成杂交探针；脾气虚证慢性胃炎与溃疡性结肠炎患者分别用Cy3标记，健康人用Cy5标记。标记好的Cy3、Cy5探针等量混匀后与cDNA芯片杂交。扫描仪扫描芯片荧光信号，处理、分析数据。分别比较脾气虚证慢性胃炎与溃疡性结肠炎患者同健康人外周血白细胞中免疫相关基因表达水平的差异。结果 脾气虚证慢性胃炎与溃疡性结肠炎患者外周血白细胞中CD9、CD164、PF4、RARB基因表达下调，IGKC、DEFA1、GNLY基因表达上调。结论 脾气虚证发生有免疫相关基因组学基础，脾虚时机体免疫功能紊乱。

Primary Exploration on Immune Associated Genome of Patients with Pi-Qi Deficiency Syndrome

ObjectiveTo investigate the abnormal change of immune function in patients with Pi-Qi deficiency Syndrome, and to explore the genomic mechanism of its genesis by cDNA chip techniques. MethodsThe cross probe was made by extracting and microamplifying the total RNA and mRNA of peripheral white blood cells (WBC) in healthy subjects and patients with chronic gastritis and ulcerative colitis, which were labeled by Cy3 and Cy5 respectively. Then equal quantity of the two labeled probes were mixed and hybridized with cDNA chip, fluorescent signal of the chips were scanned with scanner. Data obtained were analyzed for comparing the difference of the expressive levels of immune associated genome in peripheral WBC in healthy subjects with those in patients. ResultsExpressions of CD9, CD164, PF4 and RARB gene in WBC of patients, both gastritis and colitis, were down-regulated while those of IGKC, DEFA1 and GNLY were up-regulated. ConclusionThe genesis of Pi-Qi deficiency syndrome has its immune associated genomic basis, and the immune functions are disordered in patients with that syndrome.