首页> 外文期刊>Inflammation >Electro-acupuncture Pretreatment at Zusanli (ST36) Acupoint Attenuates Lipopolysaccharide-Induced Inflammation in Rats by Inhibiting Ca2+ Influx Associated with Cannabinoid CB2 Receptors
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Electro-acupuncture Pretreatment at Zusanli (ST36) Acupoint Attenuates Lipopolysaccharide-Induced Inflammation in Rats by Inhibiting Ca2+ Influx Associated with Cannabinoid CB2 Receptors

机译:Zusanli(ST36)的电针预处理(ST36)穴位通过抑制与大麻素CB2受体相关的Ca2 +流量来抑制大鼠脂多糖诱导的炎症

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摘要

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 7days 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 (Ca2+) concentration, Ca2+ influx, cannabinoid CB2 receptor (CB2R) expression, and TLR4/NF-B signaling. Our results showed EA pretreatment significantly attenuated LPS-induced inflammatory cytokine production, such as TNF-, IL-1, and IL-6. EA also enhanced CB2R expression, inhibited Ca2+ influx, and inactivated TLR4/NF-B signaling, subsequently resulting in a substantial reduction of Ca2+ 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 Ca2+ influx, and inactivate TLR4/NF-B signaling, which contributes to the alleviation of LPS-induced inflammation in rats.
机译:在这项研究中,我们旨在探讨Zusanli(ST36)穴位对脂多糖(LPS)诱导的内毒性大鼠模型的电针(EA)预处理的影响,探讨了潜在的分子机制。在ST36进行7天进行LPS,在ST36对大鼠进行大鼠。收集2小时的后LPS,诸如血清,局部穴位组织和脾脏等样品,并加工用于调查,包括细胞因子产生,细胞溶质钙(CA2 +)浓度,Ca2 +流入,大麻素CB2受体(CB2R)表达和TLR4 / NF- B信令。我们的结果表明,EA预处理显着减弱了LPS诱导的炎性细胞因子生产,例如TNF-,IL-1和IL-6。 EA还增强CB2R表达,抑制Ca2 +流入和灭活的TLR4 / NF-B信号,随后导致Ca2 +浓度的显着降低。重要的是,CB2R拮抗剂AM630有效地废除了在内毒性大鼠的ST36对ST36的抑制作用,表明CB2R参与了EA的抗炎作用。 EA预处理可以增强CB2R表达,抑制CA2 +流入,并灭活TLR4 / NF-B信号传导,这有助于减轻大鼠LPS诱导的炎症。

著录项

  • 来源
    《Inflammation》 |2019年第1期|共10页
  • 作者单位

    Hubei Univ Sch Basic Med Sci Dept Anat 1 Huangjiahu West Rd Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Chinese Med Coll Acupuncture &

    Moxibust Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Chinese Med Sch Basic Med Sci Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Sch Basic Med Sci Dept Anat 1 Huangjiahu West Rd Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Sch Basic Med Sci Dept Anat 1 Huangjiahu West Rd Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Chinese Med Coll Acupuncture &

    Moxibust Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Sch Basic Med Sci Dept Anat 1 Huangjiahu West Rd Wuhan 430065 Hubei Peoples R China;

    Hubei Univ Chinese Med Hubei Prov Collaborat Innovat Ctr Prevent Treatme 1 Huangjiahu West Rd;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 基础医学;
  • 关键词

    electro-acupuncture; lipopolysaccharide; inflammation; calcium; cannabinoid CB2 receptor; TLR4; NF-kappa B signaling;

    机译:电针;脂多糖;炎症;钙;大麻素CB2受体;TLR4;NF-Kappa发信号通知;
  • 入库时间 2022-08-20 02:16:26

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