Abstract
This study investigates the intestinal microecological mechanisms of Huoxiang Zhengqi (HXZQ) and its potential clinical applications in alleviating gastrointestinal (GI) disorders caused by cold and humid exposure. In this study, an animal model of cold exposure with GI disorders was prepared by simulating cold and humid environmental stress (CHS). Using this model, PacBio HiFi sequencing of intestinal mucosa full-length 16S rRNA and LC-MS targeted amino acid metabolomic analysis were conducted. An interaction network between the two was constructed to assess the microecological mechanism of intervention by HXZQ. Results indicate that HXZQ accelerates the recovery of GI disorders and restores the integrity of the mucus barrier in CHS mice. PacBio HiFi full-length sequencing of intestinal mucosa suggested that HXZQ can regulate the homeostasis of intestinal mucosal microbiota in CHS mice by promoting the proliferation of probiotics such as Lactobacillus reuteri (with a 6% increase in relative abundance) and inhibiting conditional pathogenic bacteria such as Helicobacter (with its relative abundance reduced to 0%). Moreover, the integrated profiling of the microbiota amino acid metabolic function and LC/MS targeted amino acid indicated that Glu and Asp are the main metabolic pathways of HXZQ intervention by intestinal mucosal microbiota in CHS mice, which is significantly associated with Lactobacillus reuteri based on the interaction network of intestinal mucosal microbiota and amino acid metabolism (P < 0.05). In conclusion, HXZQ plays a crucial role in maintaining intestinal mucosal microbiota homeostasis. By modulating the composition structure of intestinal mucosal microbiota, particularly Lactobacillus reuteri, it facilitates the restoration of Glu and Asp amino acid metabolism in the host. These effects collectively contribute to the treatment of gastrointestinal disorders induced by cold and humid environmental stress. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-025-04324-3.