Department of Anatomy, School of Basic Medical Sciences, Hubei University of Chinese Medicine, 1 Huangjiahu West Road, Hongshan District, Wuhan, 430065, China.
College of Acupuncture and Moxibustion, Hubei University of Chinese Medicine, Wuhan, 430065, China.
Inflammation. 2019 Feb;42(1):211-220. doi: 10.1007/s10753-018-0885-5.
In this study, we aimed to investigate the effect of electro-acupuncture (EA) pretreatment at zusanli (ST36) acupoint on lipopolysaccharide (LPS)-induced endotoxemic rat model and explore the underlying molecular mechanisms. Rats were treated with EA at ST36 for 7 days before being subjected to LPS. Two hours post-LPS, samples such as serum, local acupoint tissues, and spleens were collected and processed for investigations including cytokine production, cytosolic calcium (Ca) concentration, Ca influx, cannabinoid CB2 receptor (CB2R) expression, and TLR4/NF-κB signaling. Our results showed EA pretreatment significantly attenuated LPS-induced inflammatory cytokine production, such as TNF-α, IL-1β, and IL-6. EA also enhanced CB2R expression, inhibited Ca influx, and inactivated TLR4/NF-κB signaling, subsequently resulting in a substantial reduction of Ca concentration. Importantly, CB2R antagonist AM630 effectively abrogated the suppressive effect of EA at ST36 on the endotoxemic rats, suggesting CB2R was involved in the anti-inflammatory effect of EA. EA pretreatment could enhance CB2R expression, inhibit Ca influx, and inactivate TLR4/NF-κB signaling, which contributes to the alleviation of LPS-induced inflammation in rats.
在这项研究中，我们旨在探讨电针对足三里（ST36）穴位预处理对脂多糖（LPS）诱导的内毒素血症大鼠模型的影响，并探讨其潜在的分子机制。大鼠在 LPS 前用 ST36 电针治疗 7 天。在 LPS 后 2 小时，收集血清、局部穴位组织和脾脏等样本进行研究，包括细胞因子产生、细胞质钙离子（Ca）浓度、Ca 内流、大麻素 CB2 受体（CB2R）表达和 TLR4/NF-κB 信号转导。我们的结果表明，电针对 LPS 诱导的炎症细胞因子（如 TNF-α、IL-1β 和 IL-6）的产生有明显的抑制作用。电针还增强了 CB2R 的表达，抑制了 Ca 内流，并使 TLR4/NF-κB 信号失活，从而导致 Ca 浓度显著降低。重要的是，CB2R 拮抗剂 AM630 有效阻断了 ST36 电针对内毒素血症大鼠的抑制作用，表明 CB2R 参与了电针对 LPS 的抗炎作用。电针对 ST36 的预处理可以增强 CB2R 的表达，抑制 Ca 内流，使 TLR4/NF-κB 信号失活，有助于减轻 LPS 诱导的大鼠炎症。
