Han Yong-Li, Kang Zhao-Xia, Jin Shu-Wen, Pan Xiao-Li, Zhang Hong-Xing, Zhang Liang-Yu, Tang Lei
Acupuncture Department, The First Affiliated Hospital of Henan University of CM, Zhengzhou, Henan, 450003, China.
Department of Acupuncture and Moxibustion, GuiZhou University of Traditional Chinese Medicine, GuiYang, GuiZhou, 550025, China.
Heliyon. 2024 May 16;10(10):e31197. doi: 10.1016/j.heliyon.2024.e31197. eCollection 2024 May 30.
Electroacupuncture (EA) is an effective alternative for the treatment of functional dyspepsia (FD). It reduces low-grade duodenal inflammation and improves the symptoms of FD by downregulating the expression of NF-κB p65 and NLRP3, but its mechanism needs to be elucidated. To examine the regulatory effect of electroacupuncture (EA) on intestinal flora and NF-κB p65/NLRP3 pyroptosis pathway in FD rats. The FD rat model was established via multi-factor stress intervention for two weeks. The rats were randomly divided into the NC group, model group, NF-kB inhibitor group (NF-κB inhibitor BAY 11-7082 was administered), EA group, and EA + NF-kB inhibitor group. After 14 days of treatment, the rats were sacrificed, and the protein and mRNA levels of NF-κB p65, IκB, and NLRP3 in the duodenum were evaluated by Western blotting assays and real-time fluorescent quantitative PCR. The Illumina MiSeq sequencing platform was used to analyze the V4 region of the 16S rRNA gene of intestinal flora and predict functional genes. The concentration of short-chain fatty acids (SCFAs) in feces was assessed by metabolomics. EA can decrease low-grade duodenal inflammation and promote gastrointestinal motility in FD rats. This effect is mediated by inhibition of the NF-κB p65/NLRP3 pyroptosis pathway, an increase in the alpha and beta diversity of gut microbiota in the duodenum, an increase in the abundance of beneficial bacteria at the phylum and genus levels, and an increase in the content of SCFAs. The protective effect of EA against FD might involve multiple hierarchy and pathways. EA may remodel intestinal flora by inhibiting the NF-κB p65/NLRP3 pyroptosis pathway, thereby improving low-grade duodenal inflammation in FD rats.
电针是治疗功能性消化不良(FD)的一种有效替代方法。它可减轻十二指肠轻度炎症,并通过下调核因子κB(NF-κB)p65和NLRP3的表达来改善FD症状,但其机制尚需阐明。为研究电针(EA)对FD大鼠肠道菌群及NF-κB p65/NLRP3焦亡途径的调控作用。通过多因素应激干预两周建立FD大鼠模型。将大鼠随机分为正常对照组(NC组)、模型组、NF-κB抑制剂组(给予NF-κB抑制剂BAY 11-7082)、电针组和电针+NF-κB抑制剂组。治疗14天后,处死大鼠,采用蛋白质免疫印迹法和实时荧光定量PCR检测十二指肠中NF-κB p65、IκB和NLRP3的蛋白及mRNA水平。利用Illumina MiSeq测序平台分析肠道菌群16S rRNA基因的V4区,并预测功能基因。通过代谢组学评估粪便中短链脂肪酸(SCFAs)的浓度。电针可减轻FD大鼠的十二指肠轻度炎症并促进胃肠动力。这种作用是通过抑制NF-κB p65/NLRP3焦亡途径、增加十二指肠中肠道微生物群的α和β多样性、提高门和属水平有益菌的丰度以及增加SCFAs的含量来介导的。电针对FD的保护作用可能涉及多个层次和途径。电针可能通过抑制NF-κB p65/NLRP3焦亡途径重塑肠道菌群,从而改善FD大鼠的十二指肠轻度炎症。
Cell Mol Gastroenterol Hepatol. 2024
Clin Gastroenterol Hepatol. 2023-12
Nutrients. 2023-3-22
Nutrients. 2023-3-20
Biomed Pharmacother. 2023-4
Expert Rev Gastroenterol Hepatol. 2023-1