Graduate Institute of Clinical Medicine Sciences, College of Medicine, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-Shan, Tao-Yuan 333, Taiwan.
Graduate Institute of Traditional Chinese Medicine, College of Medicine, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-Shan, Tao-Yuan 333, Taiwan.
Evid Based Complement Alternat Med. 2014;2014:473978. doi: 10.1155/2014/473978. Epub 2014 Aug 17.
Suppression of white adipose tissue inflammatory signaling may contribute to the pathogenesis of obesity-induced inflammatory response. However, the precise mechanism of efficacy of acupuncture related to adipose tissue remains poorly understood. In the present study we evaluated the anti-inflammatory activities of 10 Hz electroacupuncture (EA) which was applied at the acupoint Zusanli (ST36) for 20 min per day in high-fat diet- (HFD-) induced obesity model. Treatment lasted for one week. Obese rats treated with EA showed significantly reduced body weight compared with the rats in HFD group. EA decreased the number of F4/80 and CD11b-positive macrophages in epididymal adipose tissue. We found that 10 Hz EA given 7 days/week at ST36 acupoints significantly alleviated macrophage recruitment and then improved the obesity-associated factors of sterol regulatory element-binding protein-1 (SREBP-1) and target genes expression in rats with HFD. Adipose tissue inflammatory responses indicated by tumor necrosis factor-α (TNF-α), IL-6, monocyte chemotactic protein-1 (MCP-1), and CD68 mRNA expression were significantly reduced by EA in obese rats. Additionally, EA was found to significantly reduced serum levels of TNF-α, IL-6, and IL-1 in this model. These results indicated that EA improved adipose tissue inflammatory response in obese rats, at least partly, via attenuation of lipogenesis signaling.
抑制白色脂肪组织炎症信号可能有助于肥胖引起的炎症反应的发病机制。然而,针刺相关的脂肪组织疗效的确切机制仍知之甚少。在本研究中,我们评估了每天在穴位足三里(ST36)应用 10 Hz 电针(EA)20 分钟对高脂肪饮食(HFD)诱导肥胖模型的抗炎活性。治疗持续一周。与 HFD 组的大鼠相比,接受 EA 治疗的肥胖大鼠体重明显减轻。EA 减少了附睾脂肪组织中 F4/80 和 CD11b 阳性巨噬细胞的数量。我们发现,每周 7 天在 ST36 穴位给予 10 Hz EA 可显著减轻巨噬细胞募集,从而改善 HFD 大鼠中固醇调节元件结合蛋白-1(SREBP-1)和靶基因表达的肥胖相关因素。肥胖大鼠脂肪组织炎症反应的标志物肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、单核细胞趋化蛋白-1(MCP-1)和 CD68mRNA 表达也被 EA 显著降低。此外,EA 还显著降低了该模型中 TNF-α、IL-6 和 IL-1 的血清水平。这些结果表明,EA 通过减轻脂肪生成信号通路改善了肥胖大鼠的脂肪组织炎症反应。