Auricular vagal nerve stimulation ameliorates burn-induced gastric dysmotility via sympathetic-COX-2 pathways in rats.
Auricular vagal nerve stimulation ameliorates burn-induced gastric dysmotility via sympathetic-COX-2 pathways in rats.
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DOI：
10.1111/nmo.12693
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发表时间：
2016-01
影响因子：
3.5
通讯作者：
Chen JD
中科院分区：
文献类型：
--
作者：
Li H;Yin J;Zhang Z;Winston JH;Shi XZ;Chen JD
严重的烧伤已被证明可以延缓胃排空。本研究旨在探讨耳穴电针（AEA）在迷走神经耳支支配的穴位对大鼠烧伤性胃动力障碍的影响及其细胞机制。大鼠烧伤后腹腔注射心得安（β-肾上腺素能受体拮抗剂）。所有实验均在烧伤/假烧伤后6小时进行。双侧耳穴穿刺45min。记录30min心电图。测定血浆激素；采用western blotting和实时RT-PCR检测胃组织中环氧化酶(COX)-2的表达。1)烧伤使胃排空延迟（P=0.006）， AEA使胃排空延长49% （P=0.045）。2)烧伤引起血浆去甲肾上腺素显著升高，AEA抑制了去甲肾上腺素的升高。3)烧伤显著提高胃底和胃窦COX-2蛋白和mRNA的表达。AEA抑制烧伤诱导的COX-2蛋白表达增加，但对mRNA表达无抑制作用。烧伤通过上调交感神经过度活跃导致的COX-2延迟胃排空。AEA改善烧伤引起的胃排空延迟，可能通过交感- cox -2途径介导。
Severe burn injury has been demonstrated to delay gastric emptying. The aim of this study was to investigate effects and cellular mechanisms of auricular electroacupuncture (AEA) at the acupoints innervated by the auricular branch of vagus nerve (ABVN) on burn-induced gastric dysmotility in rats. Propranolol (β-adrenoceptor antagonist) was injected intraperitoneally after the rats underwent burn injury. All experiments were performed six hours following burn/sham burn injury. AEA was performed at bilateral auricular acupoints for 45min. Electrocardiogram was recorded for 30min. Plasma hormones were measured; cyclooxygenase (COX)-2 expressions in gastric tissue were measured using western blotting and real time RT-PCR. 1) Burn injury delayed gastric emptying (P=0.006) and AEA increased gastric emptying by 49% (P=0.045). 2) Burn injury evoked a significant elevation in plasma noradrenaline, which was suppressed by AEA. 3) Burn injury significantly increased protein and mRNA expressions of COX-2 in gastric fundus and antrum. AEA suppressed burn-induced increase in protein expressions but not mRNA expressions of COX-2. Burn injury delays gastric emptying by up-regulating COX-2 attributed to sympathetic overactivity. AEA improves burn-induced delay in gastric emptying, possibly mediated via the sympathetic-COX-2 pathway.