消化性溃疡(PUD)是临床常见病、多发病。越来越多的证据表明PUD与胃肠道微生物群有关。电针(EA)是针灸的改进版本,这可以通过增加刺激和向针头输送适当的电脉冲来提高临床效果。该方法已广泛应用于消化性溃疡的治疗。然而,其对胃肠道微生物群的影响尚不清楚.因此,在本研究中,评估EA对胃十二指肠粘膜的改善作用,在PUD小鼠中评估了胃十二指肠微生物群的调节作用。将48只雄性昆明小鼠随机分为正常对照组(NC),PUD模型组(PUD),寿三里集团(LI10),和足三里组(ST36)(n=12)。分别在LI10和ST36下用EA处理组LI10和ST36中的小鼠。这种干预持续7天。随后,我们评估了胃和十二指肠粘膜的形态学变化,并测量了具体指标,包括血清多巴胺(DA)的含量,三叶因子(TFF),和血管活性肠肽(VIP)。此外,通过16S核糖体DNA测序评估了胃和十二指肠微生物群.结果表明,在LI10或ST36处的EA可显着减少PUD小鼠胃十二指肠粘膜的损伤。在与PUD模型组的微生物群落结构比较后,LI10和ST36组的胃微生物群落结构与NC组相似。此外,胃中Firmicutes的丰度减少了,而拟杆菌的数量增加了,十二指肠中Firmicutes的丰度降低。此外,LI10组胃微生物群的微生物多样性和丰富度也显著增加,ST36组血清多巴胺和三叶因子水平明显升高。因此,建议EA改善PUD与改善DA和TFF的水平以及调节胃微生物群中Firmicutes和拟杆菌的相对丰度有关。
Peptic ulcer disease (PUD) is a common disease and frequently encountered in the clinic. Accumulating evidence suggests that PUD is associated with the gastrointestinal microbiota. Electroacupuncture (EA) is an improved version of acupuncture, which can improve the clinical effect by increasing the stimulation and delivering appropriate electrical pulses to needles. This method has been widely used in the treatment of peptic ulcer disease. However, its effect on gastrointestinal microbiota remains unclear. Therefore, in the present study, the ameliorative effect of EA was evaluated on the gastroduodenal mucosa, and the regulatory effect of the gastroduodenal microbiota was assessed in PUD mice. A total of 48 male Kun Ming mice were randomly divided into the following groups: normal control group (NC), PUD model group (PUD), Shousanli group (LI10), and Zusanli group (ST36) (n=12). The mice in groups LI10 and ST36 were treated with EA at LI10 and ST36, respectively. This intervention was continued for 7 days. Subsequently, we evaluated the morphological changes in the gastric and duodenal mucosa, and specific indices were measured, including the contents of serum dopamine (DA), the trefoil factor (TFF), and the vasoactive intestinal peptide (VIP). In addition, the gastric and duodenal microbiota were assessed via 16S ribosomal DNA sequencing. The results indicated that EA at LI10 or ST36 significantly reduced the injury of the gastroduodenal mucosa in PUD mice. The gastric microbial community structure of the groups LI10 and ST36 was similar to that of the NC group following comparison with the microbial community structure of the PUD model group. Moreover, the abundance of Firmicutes in the stomach was decreased, whereas that of Bacteroidetes was increased, and the abundance of Firmicutes in the duodenum was decreased. Furthermore, the microbial diversity and richness of the gastric microbiota in group LI10 were also significantly increased, and the serum dopamine and trefoil factor levels in group ST36 were significantly increased. Therefore, it is suggested that EA ameliorating PUD is in association with improving the levels of DA and TFF and regulating the relative abundances of Firmicutes and Bacteroidetes in the gastric microbiota.