Transcutaneous auricular vagus nerve stimulation protects endotoxemic rat from lipopolysaccharide-induced inflammation.
Transcutaneous auricular vagus nerve stimulation protects endotoxemic rat from lipopolysaccharide-induced inflammation.
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经皮耳迷走神经刺激保护内毒素血症大鼠免受脂多糖诱导的炎症
DOI：
10.1155/2012/627023
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Zhu B
中科院分区：
文献类型：
--
作者：
Zhao YX;He W;Jing XH;Liu JL;Rong PJ;Ben H;Liu K;Zhu B
背景经皮耳迷走神经刺激（ta-VNS）可通过激活脑干自主神经核团引起副交感神经活动，类似于迷走神经刺激（VNS）后产生的效应。VNS通过激活胆碱能抗炎通路调节免疫功能。方法.在ST 36上进行VNS、ta-VNS或经皮穴位电刺激（TEAS）以调节炎症反应。检测内毒素血症麻醉大鼠血清中促炎细胞因子和组织中NF-κ B p65（NF-κB p65）的含量。结果与VNS作用相似，ta-VNS可抑制血清中促炎细胞因子如肿瘤坏死因子-α（TNF-α）、白细胞介素-1 β（IL-1β）、白细胞介素-6（IL-6）的水平以及肺组织NF-κ B B p65的表达。ST 36刺激还降低LPS诱导的高TNF-α水平和NF-κB信号，但其不抑制促炎细胞因子IL-1β和IL-6。ta-VNS和ST 36刺激均不能抑制迷走神经切断或注射α 7 nAChR拮抗剂后LPS诱导的TNF-α和NF-κB。结论.本研究证实ta-VNS可通过α 7 nAChR介导的胆碱能抗炎通路抑制LPS诱导的炎症反应。
Background. Transcutaneous auricular vagus nerve stimulation (ta-VNS) could evoke parasympathetic activities via activating the brainstem autonomic nuclei, similar to the effects that are produced after vagus nerve stimulation (VNS). VNS modulates immune function through activating the cholinergic anti-inflammatory pathway. Methods. VNS, ta-VNS, or transcutaneous electrical acupoint stimulation (TEAS) on ST36 was performed to modulate the inflammatory response. The concentration of serum proinflammatory cytokines and tissue NF-kappa B p65 (NF-κB p65) were detected in endotoxaemia affected anesthetized rats. Results. Similar to the effect of VNS, ta-VNS suppressed the serum proinflammatory cytokines levels, such as tumour necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) as well as NF-kappa B p65 expressions of lung tissues. ST36 stimulation also decreases LPS-induced high TNF-α level and NF-κB signal, but it did not restrain proinflammatory cytokine IL-1β and IL-6. Neither ta-VNS nor ST36 stimulation could suppress LPS-induced TNF-α and NF-κB after vagotomy or with α7nAChR antagonist injection. Conclusions. The present paper demonstrated that ta-VNS could be utilized to suppress LPS-induced inflammatory responses via α7nAChR-mediated cholinergic anti-inflammatory pathway.
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影响因子：
5.7
作者：
Hsu, CC;Weng, CS;Chang, YH
通讯作者：
Chang, YH
影响因子：
2.7
作者：
Gao, Xin-Yan;Zhang, Shi-Ping;Zhang, Hong-Qi
通讯作者：
Zhang, Hong-Qi
影响因子：
3
作者：
Li, ZY;Jiao, K;Wang, CT
通讯作者：
Wang, CT
DOI：
10.1152/ajpgi.00272.2001
发表时间：
2002-02-01
影响因子：
4.5
作者：
Ouyang, H;Yin, JY;Chen, JDZ
通讯作者：
Chen, JDZ
影响因子：
3.3
作者：
Huang, Jian;Wang, Yaoli;Huang, Xiankai
通讯作者：
Huang, Xiankai