Electroacupuncture Pretreatment Attenuates Acute Lung Injury Through α7 Nicotinic Acetylcholine Receptor-Mediated Inhibition of HMGB1 Release in Rats After Cardiopulmonary Bypass.
Electroacupuncture Pretreatment Attenuates Acute Lung Injury Through α7 Nicotinic Acetylcholine Receptor-Mediated Inhibition of HMGB1 Release in Rats After Cardiopulmonary Bypass.
复制标题
电针预处理通过a7烟碱乙酰胆碱受体介导抑制体外循环大鼠HMGB1释放减轻急性肺损伤
DOI：
10.1097/shk.0000000000001050
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发表时间：
2018-09
期刊：
影响因子：
--
通讯作者：
Yang Z
中科院分区：
文献类型：
--
作者：
Wang Z;Hou L;Yang H;Ge J;Wang S;Tian W;Wang X;Yang Z
急性肺损伤是体外循环（CPB）后常见的并发症。α7烟碱乙酰胆碱受体（nictinic acetylcholine receptor, α7nAChR）和依赖α7nAChR的胆碱能信号通路参与抑制高迁移率组盒1 （high-mobility group box 1, HMGB1）的释放和减轻炎症反应。已有研究表明，电针预处理可诱导肺损伤耐受。然而，EA在CPB中的作用尚不清楚。本研究使用EA和CPB大鼠模型来确定EA是否与CPB诱导的肺损伤有关。大鼠在“足三里（ST36）”和“肺俞（BL13）”穴位进行EA治疗5 d，然后进行CPB。cpb后2小时，处理血液、支气管肺泡灌洗液（BALF）和肺组织样本进行调查。结果表明，CPB后肺组织α7nAChR的表达明显降低。EA预处理阻止了α7nAChR表达的降低，EA预处理减少了肺水肿，抑制了CPB后血清和肺中炎症因子的释放以及BALF和HMGB1中蛋白浓度的释放，α-BGT的有益作用减弱。我们的研究表明，EA预处理对cpb诱导的ALI具有保护作用，并通过α7nAChR激活抑制大鼠HMGB1的释放。
Supplemental Digital Content is available in the text Acute lung injury is a common complication after cardiopulmonary bypass (CPB). α7 Nicotinic acetylcholine receptors (α7nAChR) and α7nAChR-dependent cholinergic signaling are implicated in suppressing the release of high-mobility group box 1 (HMGB1) and reducing the inflammatory response. A previous study has shown the electroacupuncture (EA) pretreatment induces tolerance against lung injury. However, the role of EA in CPB is poorly understood. This study used EA and a rat model of CPB to determine whether EA was associated with CPB-induced lung injury. Rats were treated with EA at “Zusanli (ST36)” and “Feishu (BL13)” acupoints for 5 days before being subjected to CPB. Two hours post-CPB, samples of blood, bronchoalveolar lavage fluid (BALF), and lung tissues were processed for investigations. Our results showed that the expression of α7nAChR in lung tissue was significantly decreased after CPB. EA pretreatment prevented the reduction in the expression of α7nAChR, EA pretreatment reduced lung edema, inhibited inflammatory cytokines release in serum and lung as well as protein concentrations in BALF and HMGB1 release after CPB, and the beneficial effects were attenuated by α-BGT. Our study demonstrates that EA pretreatment plays a protective role in CPB-induced ALI, and inhibits HMGB1 release through α7nAChR activation in rats.