Graduate Institute of Chinese Medicine, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan.
Graduate Institute of Cancer Biology, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan.
Evid Based Complement Alternat Med. 2014;2014:942196. doi: 10.1155/2014/942196. Epub 2014 Jun 9.
Inflammatory bowel disease is a chronic colonic inflammation that displays symptoms like diarrhea and weight loss. Acupuncture has been widely accepted by Western countries for the treatment of pain. Here, we analyzed efficacy and mechanism of electroacupuncture (EA) on trinitrobenzene sulfonic acid- (TNBS-) induced colitis in mice. Mice were intrarectally administered with 250 mg/kg TNBS and electroacupunctured at Quze (PC3) and Neiguan (PC6) acupoints, which have been applied for gastrointestinal disorders. Gene expression profiles in colons and spleens were analyzed by microarray for the elucidation of mechanism of EA. Our data showed that EA at PC3 and PC6 improved macroscopic and microscopic features of colitis and the improvement displayed a frequency-dependent manner. Administration of TNBS upregulated the expression of most cytokine genes in colons, while EA downregulated the expression of TNBS-induced cytokine genes. Pathway analysis showed that EA significantly affected inflammatory pathways in colons and immunity-associated pathway in spleens. Immunohistochemical staining further showed that EA decreased the expression of interleukin-1 β and nuclear factor- κ B. In conclusion, this is the first study reporting the global gene expression profiles of EA on TNBS-induced colitis. Our findings suggested that inflammatory and immunity pathways were involved in the anti-inflammatory mechanism of EA on colitis induced by TNBS.
炎症性肠病是一种慢性结肠炎症，表现为腹泻和体重减轻等症状。针灸已被西方国家广泛接受，用于治疗疼痛。在这里，我们分析了电针对三硝基苯磺酸-（TNBS-）诱导的小鼠结肠炎的疗效和机制。小鼠经直肠给予 250mg/kg TNBS，并在曲泽（PC3）和内关（PC6）穴位进行电针治疗，这些穴位已应用于胃肠道疾病。通过微阵列分析结肠和脾脏中的基因表达谱，以阐明 EA 的作用机制。我们的数据表明，PC3 和 PC6 处的 EA 改善了结肠炎的宏观和微观特征，并且这种改善呈现出频率依赖性。TNBS 的给药上调了结肠中大多数细胞因子基因的表达，而 EA 下调了 TNBS 诱导的细胞因子基因的表达。通路分析表明，EA 显著影响了结肠中的炎症通路和脾脏中的免疫相关通路。免疫组织化学染色进一步表明，EA 降低了白细胞介素-1β和核因子-κB 的表达。总之，这是第一项报道 EA 对 TNBS 诱导的结肠炎的全基因表达谱的研究。我们的研究结果表明，炎症和免疫通路参与了 EA 对 TNBS 诱导的结肠炎的抗炎机制。
