Electroacupuncture with different current intensities can improve gastrointestinal motility in diabetic gastroparesis via vagal and sympathetic pathways.
Yi-Wen Tang, You Zhang, Jin Zhou, Yu-Ting Peng, Yan Zi, Yan-Rong Wei, Zeng-Hui Yue
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引用次数: 0
Abstract
Background: Diabetic gastroparesis (DGP) disrupts gastric motility. Electroacupuncture (EA) at Zusanli (ST36) may alleviate DGP symptoms via neural pathways.
Aim: To investigate how EA current intensities at ST36 regulate neural pathways and improve gastric motility in DGP models.
Methods: A DGP model was established using intraperitoneal injection of streptozotocin. Gastrointestinal motility was measured in rats after 2 weeks of continuous EA at ST36. Current intensity was selected as 0.5 mA, 1 mA, and 3 mA. Gastric electrodynamics were detected by recording and analyzing the number of gastric discharges. The gastric emptying rate and propulsion rate of the small intestine were measured to assess dynamic gastrointestinal function. Hematoxylin-eosin staining was conducted to measure histopathological changes in the gastric sinus. Reverse transcription-polymerase chain reaction was conducted to determine mRNA levels of Rho guanine nucleotide-binding protein A and Rho-associated coiled-coil forming protein kinase. Western blotting was conducted to determine the expression levels of choline acetyltransferase, tyrosine hydroxylase, Rho guanine nucleotide-binding protein A, and Rho-associated coiled-coil forming protein kinase. Immunofluorescence staining in the stomach was conducted to detect the distribution of C-kit, an interstitial cell of Cajal marker. An enzyme-linked immunosorbent assay was conducted to detect serum levels of acetylcholine and norepinephrine.
Results: Treatment with EA improved gastric emptying and gastric smooth muscle disorders in rats with DGP, mitigated pathological damage, and restored the function of interstitial cells of Cajal. In addition, different current intensities of EA affected gastrointestinal function of rats with DGP. The 0.5 mA, 1 mA, and 3 mA EA groups all improved gastrointestinal function. 0.5 mA EA increased acetylcholine levels by increasing protein expression of choline acetyltransferase (P < 0.05), thereby upregulating vagus nerve activity and enhancing parasympathetic nerve regulation. 3 mA EA increased norepinephrine levels (P < 0.05) by increasing protein expression of tyrosine hydroxylase, thereby activating the sympathetic nervous pathway. 1 mA coordinated the function of the vagus and sympathetic nerves to improve gastrointestinal motility.
Conclusion: EA with ST36 improved gastric motility in rats with DGP. 0.5 mA EA activated the vagus nerve, while 3 mA EA regulated gastrointestinal motility by activating the sympathetic nerves.
背景：糖尿病性胃轻瘫（DGP）破坏胃运动。电针足三里（ST36）可通过神经通路缓解DGP症状。目的：探讨EA电流强度对胃粘膜生长阻滞模型ST36神经通路的调节作用及对胃运动的改善作用。方法：采用链脲佐菌素腹腔注射建立DGP模型。在ST36连续EA治疗2周后测量大鼠胃肠运动。电流强度分别为0.5 mA、1ma和3ma。通过记录和分析胃分泌物的次数来检测胃电动力学。测定胃排空率和小肠推进率，评估动态胃肠功能。采用苏木精-伊红染色法测定胃窦组织病理变化。逆转录-聚合酶链反应测定Rho鸟嘌呤核苷酸结合蛋白A和Rho相关的卷曲卷曲形成蛋白激酶的mRNA水平。Western blotting检测胆碱乙酰转移酶、酪氨酸羟化酶、Rho鸟嘌呤核苷酸结合蛋白A、Rho相关卷曲形成蛋白激酶的表达水平。采用免疫荧光染色法检测胃Cajal标志物间质细胞C-kit的分布。采用酶联免疫吸附法检测血清乙酰胆碱和去甲肾上腺素水平。结果：EA能改善DGP大鼠胃排空及胃平滑肌功能紊乱，减轻病理损伤，恢复Cajal间质细胞功能。此外，不同电流强度的EA对DGP大鼠的胃肠功能也有影响。0.5 mA、1 mA和3 mA EA组均能改善胃肠功能。0.5 mA EA通过增加胆碱乙酰转移酶蛋白表达增加乙酰胆碱水平（P < 0.05），从而上调迷走神经活性，增强副交感神经调节。3 mA EA通过增加酪氨酸羟化酶蛋白表达，激活交感神经通路，使去甲肾上腺素水平升高（P < 0.05）。mA协调迷走神经和交感神经的功能，改善胃肠运动。结论：ST36加EA可改善DGP大鼠的胃动力。0.5 mA EA激活迷走神经，而3 mA EA通过激活交感神经调节胃肠运动。
期刊介绍：
The WJD is a high-quality, peer reviewed, open-access journal. The primary task of WJD is to rapidly publish high-quality original articles, reviews, editorials, and case reports in the field of diabetes. In order to promote productive academic communication, the peer review process for the WJD is transparent; to this end, all published manuscripts are accompanied by the anonymized reviewers’ comments as well as the authors’ responses. The primary aims of the WJD are to improve diagnostic, therapeutic and preventive modalities and the skills of clinicians and to guide clinical practice in diabetes. Scope: Diabetes Complications, Experimental Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Diabetes, Gestational, Diabetic Angiopathies, Diabetic Cardiomyopathies, Diabetic Coma, Diabetic Ketoacidosis, Diabetic Nephropathies, Diabetic Neuropathies, Donohue Syndrome, Fetal Macrosomia, and Prediabetic State.
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