Rehabilitation Department, Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Acumoxa, Wuhan Integrated TCM & Western Medicine Hospital, Wuhan, China.
Dig Dis Sci. 2020 Jun;65(6):1689-1699. doi: 10.1007/s10620-019-05960-5. Epub 2019 Dec 21.
Gastrointestinal motility disorder is an important pathological basis for functional dyspepsia (FD). Epigastric ache and discomfort are the main symptoms of FD, and ghrelin deficiency is closely related to the occurrence and development of FD. While electroacupuncture (EA) alleviated the symptoms of FD patients and improved their quality of life, there is a lack of sufficient mechanistic evidence to support these beneficial effects.
An in vivo FD model was established in wild-type and mammalian target of rapamycin (mTOR) knockout (-/-) rats. FD rats were subjected to EA with or without mTOR agonists or inhibitors. Gastric emptying and intestinal propulsion were assessed, and pathological changes in the hypothalamus, gastric antrum, and small intestine were examined histologically. In addition, ghrelin expression and AMPK/TSC2/Rheb/mTOR activation were detected by quantitative reverse transcription polymerase chain reaction and western blot.
EA alone or in combination with mTOR inhibitors improved gastrointestinal function in FD rats by increasing the rates of intestinal propulsion and gastric emptying, and pathological changes in the hypothalamus, gastric antrum, and small intestine were alleviated. This may be related to the significant upregulation of ghrelin expression and the effective activation of the AMPK/TSC2/Rheb/mTOR signaling pathway. Interestingly, EA also improved gastrointestinal function and ghrelin expression in mTOR (-/-) KO FD rats.
Altering the level of ghrelin by regulating AMPK/TSC2/Rheb-mediated mTOR inhibition is an important way through which EA treats FD. The complex EA-mediated regulatory mechanisms of the brain-gut axis still require further exploration.
胃肠动力障碍是功能性消化不良（FD）的重要病理基础。上腹痛和不适是 FD 的主要症状，而胃饥饿素缺乏与 FD 的发生和发展密切相关。电针（EA）缓解了 FD 患者的症状，提高了他们的生活质量，但缺乏足够的机制证据来支持这些有益的影响。
建立野生型和哺乳动物雷帕霉素靶蛋白（mTOR）敲除（-/-）大鼠体内 FD 模型。FD 大鼠接受 EA 治疗，或与 mTOR 激动剂或抑制剂联合治疗。评估胃排空和肠推进，通过组织学检查下丘脑、胃窦和小肠的病理变化。此外，通过定量逆转录聚合酶链反应和 Western blot 检测胃饥饿素表达和 AMPK/TSC2/Rheb/mTOR 激活。
EA 单独或与 mTOR 抑制剂联合使用可通过增加肠推进率和胃排空率来改善 FD 大鼠的胃肠功能，并缓解下丘脑、胃窦和小肠的病理变化。这可能与胃饥饿素表达的显著上调和 AMPK/TSC2/Rheb/mTOR 信号通路的有效激活有关。有趣的是，EA 还改善了 mTOR（-/-）KO FD 大鼠的胃肠功能和胃饥饿素表达。
通过调节 AMPK/TSC2/Rheb 介导的 mTOR 抑制来改变胃饥饿素水平是 EA 治疗 FD 的重要途径。脑-肠轴的复杂 EA 调节机制仍需要进一步探索。
