Department of Physiology, College of Oriental Medicine, Kyung Hee University, #1 Hoegi-dong, Dongdaemoon-gu, Seoul 130-701, Republic of Korea.
Evid Based Complement Alternat Med. 2011;2011:508689. doi: 10.1093/ecam/nep222. Epub 2011 Jun 5.
Clinical evidence indicates that electroacupuncture (EA) is effective for allergic disorder. Recent animal studies have shown that EA treatment reduces levels of IgE and Th2 cytokines in BALB/c mice immunized with 2,4-dinitrophenylated keyhole limpet protein (DNP-KLH). The hypothalamus, a brain center of the neural-immune system, is known to be activated by EA stimulation. This study was performed to identify and characterize the differentially expressed genes in the hypothalamus of DNP-KLH immunized mice that were stimulated with EA or only restrained. To this aim, we conducted a microarray analysis to evaluate the global gene expression profiles, using the hypothalamic RNA samples taken from three groups of mice: (i) normal control group (no treatments); (ii) IMH group (DNP-KLH immunization + restraint); and (iii) IMEA group (immunization + EA stimulation). The microarray analysis revealed that total 39 genes were altered in their expression levels by EA treatment. Ten genes, including T-cell receptor alpha variable region family 13 subfamily 1 (Tcra-V13.1), heat shock protein 1B (Hspa1b) and 2'-5' oligoadenylate synthetase 1F (Oas1f), were up-regulated in the IMEA group when compared with the IMH group. In contrast, 29 genes, including decay accelerating factor 2 (Daf2), NAD(P)H dehydrogenase, quinone 1 (Nqo1) and programmed cell death 1 ligand 2 (Pdcd1lg2) were down-regulated in the IMEA group as compared with the IMH group. These results suggest that EA treatment can modulate immune response in DNP-KLH immunized mice by regulating expression levels of genes that are associated with innate immune, cellular defense and/or other kinds of immune system in the hypothalamus.
临床证据表明，电针（EA）对过敏性疾病有效。最近的动物研究表明，电针治疗可降低 2,4-二硝基苯化钥孔血蓝蛋白（DNP-KLH）免疫的 BALB/c 小鼠的 IgE 和 Th2 细胞因子水平。下丘脑是神经-免疫系统的脑中枢，已知可被 EA 刺激激活。本研究旨在鉴定和表征经 EA 刺激或仅束缚的 DNP-KLH 免疫小鼠下丘脑的差异表达基因。为此，我们进行了微阵列分析，使用来自三组小鼠的下丘脑 RNA 样本评估了全基因表达谱：（i）正常对照组（无处理）；（ii）IMH 组（DNP-KLH 免疫+束缚）；和（iii）IMEA 组（免疫+EA 刺激）。微阵列分析显示，EA 处理共改变了 39 个基因的表达水平。与 IMH 组相比，IMEA 组中有 10 个基因（包括 T 细胞受体α可变区家族 13 亚家族 1（Tcra-V13.1）、热休克蛋白 1B（Hspa1b）和 2'-5'寡聚腺苷酸合成酶 1F（Oas1f））的表达上调。相比之下，IMEA 组中有 29 个基因（包括衰减加速因子 2（Daf2）、NAD（P）H 脱氢酶醌 1（Nqo1）和程序性细胞死亡 1 配体 2（Pdcd1lg2））的表达下调与 IMH 组相比。这些结果表明，EA 治疗可通过调节与下丘脑固有免疫、细胞防御和/或其他类型免疫系统相关的基因表达水平来调节 DNP-KLH 免疫小鼠的免疫反应。
