首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Electrical Stimulation at the ST36 Acupoint Protects against Sepsis Lethality and Reduces Serum TNF Levels through Vagus Nerve- and Catecholamine-Dependent Mechanisms
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Electrical Stimulation at the ST36 Acupoint Protects against Sepsis Lethality and Reduces Serum TNF Levels through Vagus Nerve- and Catecholamine-Dependent Mechanisms

机译:ST36穴位的电刺激可通过迷走神经和儿茶酚胺依赖性机制预防败血症致命性并降低血清TNF水平

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摘要

Electrical vagus nerve (VN) stimulation during sepsis attenuates tumor necrosis factor (TNF) production through the cholinergic anti-inflammatory pathway, which depends on the integrity of the VN and catecholamine production. To characterize the effect of electroacupuncture at ST36 (EA-ST36) on serum TNF, IL-6, nitrite, and HMGB1 levels and survival rates, based on VN integrity and catecholamine production, a sepsis model was induced in rats using cecal ligation and puncture (CLP). The septic rats were subsequently treated with EA-ST36 (CLP+ST36), and serum samples were collected and analyzed for cytokines levels. The serum TNF, IL-6, nitrite, and HMGB1 levels in the CLP+ST36 group were significantly lower compared with the group without treatment, the survival rates were significantly higher (P < 0.05), and the acute organ injury induced by CLP was mitigated by EA-ST36; however, when subdiaphragmatic vagotomy was performed, the serum levels of TNF in the CLP+ST36 group did not show a significant difference compared with the group without electrostimulation, and, similarly, no significant difference in serum TNF levels was found under the pharmacological blockade of catecholamines. These results suggest that in rats with CLP sepsis models EA-ST36 reduces serum TNF levels through VN- and atecholamine-dependent mechanisms.
机译:败血症期间电迷走神经(VN)刺激通过胆碱能抗炎途径减弱了肿瘤坏死因子(TNF)的产生,这取决于VN的完整性和儿茶酚胺的产生。为了表征电针在ST36(EA-ST36)上对血清TNF,IL-6,亚硝酸盐和HMGB1水平和存活率的影响,基于VN完整性和儿茶酚胺的产生,使用盲肠结扎和穿刺法在大鼠中诱发败血症模型(CLP)。随后用EA-ST36(CLP + ST36)处理败血大鼠,并收集血清样品并分析细胞因子水平。与未经治疗的组相比,CLP + ST36组的血清TNF,IL-6,亚硝酸盐和HMGB1水平显着降低,存活率显着更高(P <0.05),CLP引起的急性器官损伤为由EA-ST36减轻;然而,当进行ph肌下迷走神经切断术时,CLP + ST36组的血清TNF水平与未电刺激组相比无显着差异,并且类似地,在LP的药理学阻断作用下,血清TNF水平也无显着差异。儿茶酚胺。这些结果表明,在患有CLP败血症模型的大鼠中,EA-ST36通过VN和邻苯二酚依赖性机制降低血清TNF水平。

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