[Mechanism of Quzhou Aurantii Fructus in treating rats with functional dyspepsia based on gut microbiota and metabolomics].

Both QAFA and AFA increased gastrointestinal motility in functional dyspepsia rats.

• FD rat models were constructed by a combined method of 'pinching tail + irregular diet + drinking dilute acidic water'
• QAFA was administered orally at a dose of 2.05 g·kg⁻¹ (equivalent to 4 g·kg⁻¹ QAF)
• AFA was administered orally at a dose of 1.93 g·kg⁻¹ (equivalent to 4 g·kg⁻¹ AF)
• Treatment duration was 14 days, after which gastric emptying and intestinal propulsion were assessed

Both QAFA and AFA repaired the damaged intestinal barrier in FD rats.

• Intestinal barrier repair was assessed via hematoxylin-eosin (HE) staining and immunofluorescence analysis
• Pathological changes in the gastric antrum and duodenum were analyzed via histology
• Both treatments showed restoration of intestinal barrier integrity compared to FD model rats

Both QAFA and AFA regulated serum levels of gastrin (GAS) and vasoactive intestinal polypeptide (VIP) in FD rats.

• GAS and VIP levels were measured by enzyme-linked immunosorbent assay (ELISA)
• Regulation of these gastrointestinal hormones was identified as part of the mechanism by which both extracts improve FD symptoms
• Both GAS and VIP are key markers of gastrointestinal function and motility regulation

Both QAFA and AFA reduced the abundance of the harmful microbe Ruminococcus in FD rats.

• Gut microbiota composition was assessed using 16S rRNA sequencing
• Reduction of Ruminococcus was a shared mechanism between both QAFA and AFA treatments
• Correlation analysis between metabolites and gut microbiota confirmed that decreased Ruminococcus abundance was associated with restored serum metabolite levels for both treatments

AFA and QAFA differed in the specific beneficial bacteria they increased, with AFA increasing Prevotella and Lactobacillus, while QAFA increased Clostridia UCG-014.

• AFA increased the abundance of the beneficial bacteria Prevotella and Lactobacillus
• QAFA increased the abundance of Clostridia UCG-014
• Correlation analysis showed AFA increased Prevotella abundance, which contributed to restoring serum metabolite levels
• These differences indicate that QAFA and AFA have distinct but overlapping mechanisms of action on gut microbiota

Both QAFA and AFA restored serum metabolites primarily through regulating phospholipid metabolism.

• Serum metabolomics analysis was used to identify affected metabolic pathways
• Phospholipid metabolism was identified as the primary metabolic pathway modulated by both treatments
• Metabolite-gut microbiota correlation analysis linked changes in specific microbial taxa to restoration of serum metabolite levels
• Both treatments showed restoration of disturbed serum metabolite profiles toward normal levels