Tang Yi-Wen, Zhang You, Zhou Jin, Peng Yu-Ting, Zi Yan, Wei Yan-Rong, Yue Zeng-Hui
College of Acupuncture, Massage and Rehabilitation, Hunan University of Chinese Medicine, Changsha 410208, Hunan Province, China.
World J Diabetes. 2025 Aug 15;16(8):107779. doi: 10.4239/wjd.v16.i8.107779.
Diabetic gastroparesis (DGP) disrupts gastric motility. Electroacupuncture (EA) at Zusanli (ST36) may alleviate DGP symptoms neural pathways.
To investigate how EA current intensities at ST36 regulate neural pathways and improve gastric motility in DGP models.
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.
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 ( < 0.05), thereby upregulating vagus nerve activity and enhancing parasympathetic nerve regulation. 3 mA EA increased norepinephrine levels ( < 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.
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.
糖尿病胃轻瘫（DGP）会扰乱胃动力。针刺足三里（ST36）可能通过神经通路缓解DGP症状。
探讨ST36处的电针电流强度如何调节神经通路并改善DGP模型中的胃动力。
通过腹腔注射链脲佐菌素建立DGP模型。在对ST36连续电针2周后，测量大鼠的胃肠动力。电流强度分别选择为0.5 mA、1 mA和3 mA。通过记录和分析胃电活动次数来检测胃电动力学。测量胃排空率和小肠推进率以评估胃肠动态功能。进行苏木精-伊红染色以测量胃窦的组织病理学变化。进行逆转录-聚合酶链反应以测定Rho鸟嘌呤核苷酸结合蛋白A和Rho相关卷曲螺旋形成蛋白激酶的mRNA水平。进行蛋白质印迹法以测定胆碱乙酰转移酶、酪氨酸羟化酶、Rho鸟嘌呤核苷酸结合蛋白A和Rho相关卷曲螺旋形成蛋白激酶的表达水平。在胃中进行免疫荧光染色以检测Cajal间质细胞标志物C-kit的分布。进行酶联免疫吸附测定以检测血清乙酰胆碱和去甲肾上腺素水平。
电针治疗改善了DGP大鼠的胃排空和胃平滑肌紊乱，减轻了病理损伤，并恢复了Cajal间质细胞的功能。此外，不同电流强度的电针对DGP大鼠的胃肠功能有影响。0.5 mA、1 mA和3 mA电针组均改善了胃肠功能。0.5 mA电针通过增加胆碱乙酰转移酶的蛋白表达来提高乙酰胆碱水平（<0.05），从而上调迷走神经活性并增强副交感神经调节。3 mA电针通过增加酪氨酸羟化酶的蛋白表达来提高去甲肾上腺素水平（<0.05），从而激活交感神经通路。1 mA协调迷走神经和交感神经的功能以改善胃肠动力。
针刺ST36改善了DGP大鼠的胃动力。0.5 mA电针激活迷走神经，而3 mA电针通过激活交感神经调节胃肠动力。
